autoimmune disease
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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2014/07/04 23:48:39」(JST)
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[Wiki en表示]Autoimmune diseases | |
---|---|
Classification and external resources | |
ICD-10 | D84.9, M35.9 |
ICD-9 | 279.4 |
OMIM | 109100 |
DiseasesDB | 28805 |
MedlinePlus | 000816 |
MeSH | D001327 |
Autoimmune diseases arise from an abnormal immune response of the body against substances and tissues normally present in the body (autoimmunity). This may be restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue in different places (e.g. Goodpasture's disease which may affect the basement membrane in both the lung and the kidney). The treatment of autoimmune diseases is typically with immunosuppression—medication that decreases the immune response. A large number of autoimmune diseases are recognized. A major understanding of the underlying pathophysiology of autoimmune diseases has been the application of genome wide association scans that have identified a striking degree of genetic sharing among the autoimmune diseases.[1]
Contents
- 1 Criteria
- 2 Effects
- 3 Classification
- 4 Development of therapies
- 5 See also
- 6 References
- 7 Further reading
- 8 External links
Criteria
For a disease to be regarded as an autoimmune disease it needs to answer to Witebsky's postulates (first formulated by Ernst Witebsky and colleagues in 1957 and modified in 1994):[2][3]
- Direct evidence from transfer of pathogenic antibody or pathogenic T cells
- Indirect evidence based on reproduction of the autoimmune disease in experimental animals
- Circumstantial evidence from clinical clues
- Genetic architecture clustering with other autoimmune diseases
Effects
It has been estimated that autoimmune diseases are among the ten leading causes of death among women in all age groups up to 65 years.[4]
A substantial minority of the population suffers from these diseases, which are often chronic, debilitating, and life-threatening. There are more than eighty illnesses caused by autoimmunity.[5]
Classification
It is possible to classify autoimmune diseases by corresponding type of hypersensitivity: type II, type III, or type IV. (No type of autoimmune disease mimics type I hypersensitivity.)[6]
There is continuing debate about when a disease should be considered autoimmune, leading to different criteria such as Witebsky's postulates.
Name: | Accepted/ suspected |
Hypersensitivity
I, II, III, IV |
Autoantibody | Notes | |
---|---|---|---|---|---|
Acute disseminated encephalomyelitis (ADEM) | Accepted[7] | ||||
Addison's disease | interferon omega; transglutaminase; aromatic acid carboxylase; GAD; HAI; 17 hydroxylase; 21 hydroxylase | ||||
Agammaglobulinemia | IGHM; IGLL1: CD79A; CD79B; BLNK; LRRC8A | ||||
Alopecia areata | Accepted[8][9] | T-cells | |||
Amyotrophic lateral sclerosis (Also Lou Gehrig's disease; Motor Neuron Disease) | VCP, ATXN2, OPTN, FIG4, TARDBP, ANG, VAPB, FUS, SETX, ALS2, SOD1 | ||||
Ankylosing Spondylitis | Suspected[10][11] | CD8; HLA-B27 | |||
Antiphospholipid syndrome | Accepted[7] | anti-cardiolipin;anti pyruvate dehydrogenase; β2 glycoprotein I; phosphatidylserine; anti apoH; Annexin A5 | HLA-DR7, HLA-B8, HLA-DR2, HLA-DR3 | ||
Antisynthetase syndrome | |||||
Atopic allergy | I | ||||
Atopic dermatitis | I | ||||
Autoimmune aplastic anemia | |||||
Autoimmune cardiomyopathy | Accepted | ||||
Autoimmune enteropathy | |||||
Autoimmune hemolytic anemia | Accepted | II | complement activation | ||
Autoimmune hepatitis | Accepted | cell-mediated | anti-mitochondrial antibodies; ANA; anti-smooth muscle antibodies, LKM-1; soluble liver antigen | ||
Autoimmune inner ear disease | Accepted | [12] | |||
Autoimmune lymphoproliferative syndrome | Accepted | TNFRSF6; defective Fas-CD95 apoptosis | |||
Autoimmune peripheral neuropathy | Accepted | ||||
Autoimmune pancreatitis | Accepted | ANA; anti-lactoferrin antibodiesanti-carbonic anhydrase antibodies; rheumatoid factor | |||
Autoimmune polyendocrine syndrome | Accepted | Unknown or multiple | APS-1 see Addison's disease | ||
Autoimmune progesterone dermatitis | Accepted | ||||
Autoimmune thrombocytopenic purpura | Accepted | anti gpIIb-IIIa or 1b-IX | |||
Autoimmune urticaria | Accepted | [13] | |||
Autoimmune uveitis | Accepted | HLAB-27? | |||
Balo disease/Balo concentric sclerosis | |||||
Behçet's disease | Accepted | immune-mediated systemic vasculitis; linkage to HLA-B51 (HLA-B27); very different manifestations with ulcers as common symptom; also called Morbus Adamandiades-Behçet | |||
Berger's disease | IgA (elevated in 50% of patients), IgA (in mesangial deposits on kidney biopsy) | ||||
Bickerstaff's encephalitis | Anti-GQ1b 2/3 patients | similar to Guillain-Barré syndrome | |||
Blau syndrome | overlaps both sarcoidosis and granuloma annulare | ||||
Bullous pemphigoid | IgG autoantibodies targeting the type XVII collagen component of hemidesmosomes | [14] | |||
Cancer | |||||
Castleman's disease | Over expression of IL-6 | ||||
Celiac disease | Accepted[15][16][17] | IV?? | Anti-tissue transglutaminase antibodies anti-endomysial IgA, anti-gliadin IgA | HLA-DQ8 and DQ2.5 | |
Chagas disease | Suspected[18] | ||||
Chronic inflammatory demyelinating polyneuropathy | Anti-ganglioside antibodies:anti-GM1, anti-GD1a, anti-GQ1b | similar to Guillain-Barré syndrome | |||
Chronic recurrent multifocal osteomyelitis | LPIN2, D18S60,similar to Majeed syndrome | ||||
Chronic obstructive pulmonary disease | Suspected[19][20] | ||||
Churg-Strauss syndrome | p-ANCA Eosinophilia[21] | ||||
Cicatricial pemphigoid | anti-BP-1, anti BP-2 | precipitates C3 | |||
Cogan syndrome | |||||
Cold agglutinin disease | Accepted | II | IgM | idiopathic or secondary to leukemia or infection | |
Complement component 2 deficiency | |||||
Contact dermatitis | IV | ||||
Cranial arteritis | aka Temporal arteritis; involves giant cells | ||||
CREST syndrome | Anti-centromere antibodies Anti-nuclear antibodies | ||||
Crohn's disease | Immune related[22] | IV | Innate immunity; Th17; Th1; ATG16L1; CARD15;XBP1; | ||
Cushing's Syndrome | cortisol binding globulin? | ||||
Cutaneous leukocytoclastic angiitis | neutrophils | ||||
Dego's disease | Vasculopathy | ||||
Dercum's disease | Suspected | Lipoid tissue.[23] | |||
Dermatitis herpetiformis | IgA Eosinophilia;[21] anti-epidermal transglutaminase antibodies | ||||
Dermatomyositis | Accepted[24] | histidine-tRNA anti-signal recognition peptide Anti-Mi-2 Anti-Jo1.[25] | B- and T-cell perivascular inflammatory infiltrate on muscle biopsy | ||
Diabetes mellitus type 1 | Accepted[7] | IV | Glutamic acid decarboxylase antibodies (GADA), islet cell antibodies (ICA), and insulinoma-associated autoantibodies (IA-2), anti-insulin antibodies | HLA-DR3, HLA-DR4 | |
Diffuse cutaneous systemic sclerosis | anti-nuclear antibodies, anti-centromere and anti-scl70/anti-topoisomerase antibodies[26] | COL1A2 and TGF-β1 | |||
Dressler's syndrome | myocardial neo-antigens formed as a result of the MI | ||||
Drug-induced lupus | Anti-histone antibodies | ||||
Discoid lupus erythematosus | III | IL-2 and IFN-gamma>[27] | |||
Eczema | LEKTI, SPINK5,[28] filaggrin.,[29] Brain-derived neurotrophic factor (BDNF) and Substance P.[30] | ||||
Endometriosis | Suspected[31] | ||||
Enthesitis-related arthritis[32] | . | MMP3[33] TRLR2, TLR4,[34] ERAP1[35] | |||
Eosinophilic fasciitis | Accepted | ||||
Eosinophilic gastroenteritis | IgE | IL-3, IL-5, GM-CSF, eotaxin | |||
Eosinophilic pneumonia | |||||
Epidermolysis bullosa acquisita | COL7A1 | ||||
Erythema nodosum | |||||
Erythroblastosis fetalis | II | ABO, Rh, Kell antibodies | mother's immune system attacks fetus | ||
Essential mixed cryoglobulinemia | |||||
Evan's syndrome | |||||
Fibrodysplasia ossificans progressiva | ACVR1 Lymphocytes express increased BMP4 | ||||
Fibrosing alveolitis (or Idiopathic pulmonary fibrosis) | SFTPA1, SFTPA2, TERT, and TERC.[36] | ||||
Gastritis | serum antiparietal and anti-IF antibodies | ||||
Gastrointestinal pemphigoid | Accepted | ||||
Glomerulonephritis | Sometimes | IgA | see Buerger's disease for IgA; Membranous glomerulonephritis for IgG; Membranoproliferative/mesangiocapillary GN (Complement activation); Goodpasture's syndrome; Wegener's granulomatosis | ||
Goodpasture's syndrome | Accepted[7] | II | Anti-Basement Membrane Collagen Type IV Protein | ||
Graves' disease | Accepted[7] | II | thyroid autoantibodies (TSHR-Ab) that activate the TSH-receptor (TSHR) | ||
Guillain-Barré syndrome (GBS) | Accepted[7] | IV | Anti-ganglioside | ||
Hashimoto's encephalopathy | Accepted[7] | IV | alpha-enolase[37] | ||
Hashimoto's thyroiditis | Accepted[7] | IV | antibodies against thyroid peroxidase and/or thyroglobulin | HLADR5, CTLA-4 | |
Henoch-Schonlein purpura | immunoglobulin A (IgA) and complement component 3 (C3) | ||||
Herpes gestationis aka Gestational Pemphigoid | IgG and C3 misdirected antibodies intended to protect the placenta | ||||
Hidradenitis suppurativa | Suspected[38] | ||||
Hughes-Stovin syndrome | |||||
Hypogammaglobulinemia | IGHM, IGLL1, CD79A, BLNK, LRRC8A, CD79B | ||||
Idiopathic inflammatory demyelinating diseases | a variant of multiple sclerosis | ||||
Idiopathic pulmonary fibrosis | SFTPA1, SFTPA2, TERT, and TERC.[36] | ||||
Idiopathic thrombocytopenic purpura (See Autoimmune thrombocytopenic purpura) | Accepted[7] | II | glycoproteins IIb-IIIa or Ib-IX, immunoglobulin G | ||
IgA nephropathy | III? | IgA produced from marrow rather than MALT | |||
Inclusion body myositis | similar to polymyositis but does not respond to steroid therapy-activated T8 cells | ||||
Chronic inflammatory demyelinating polyneuropathy | anti-ganglioside antibodies | similar to Guillain–Barré syndrome | |||
Interstitial cystitis | Suspected[39] | Mast cells | |||
Juvenile idiopathic arthritis aka Juvenile rheumatoid arthritis | inconsistent ANA Rheumatoid factor | ||||
Kawasaki's disease | Suspected | ITPKC HLA-B51 | |||
Lambert-Eaton myasthenic syndrome | voltage-gated calcium channels; Q-type calcium channel, synaptogagmin, muscarinic acetylcholine receptor M1 | HLA-DR3-B8 | |||
Leukocytoclastic vasculitis | |||||
Lichen planus | |||||
Lichen sclerosus | |||||
Linear IgA disease (LAD) | |||||
Lupoid hepatitis aka Autoimmune hepatitis | ANA and SMA,[40] LKM-1, LKM-2 or LKM-3; antibodies against soluble liver antigen[41][42] (anti-SLA, anti-LP) no autoantibodies detected (~20%)[citation needed] | ||||
Lupus erythematosus | Accepted[7] | III | Anti-nuclear antibodies[43] anti-Ro.[44] Also, they are often present in Sjögren's syndrome.[45][46]Eosinophilia[21] | ||
Majeed syndrome | LPIN2 | ||||
Ménière's disease | III? | major peripheral myelin protein P0[47] | |||
Microscopic polyangiitis | p-ANCA myeloperoxidase | binds to neutrophils causing them to degranulate and damages endothelium | |||
Miller-Fisher syndrome see Guillain-Barre Syndrome | Accepted | anti-GQ1b | |||
Mixed connective tissue disease | Accepted[7] | anti-nuclear antibody anti-U1-RNP | HLA-DR4 | ||
Morphea | Suspected[48] | ||||
Mucha-Habermann disease aka Pityriasis lichenoides et varioliformis acuta | T-cells | ||||
Multiple sclerosis | Accepted[49] | IV | Anti-Kir4.1 (heterogeneous)[49] | Autoantibody against potasium channel. Also invoved HLA-DR2, PECAM-1[50] Anti-myelin basic protein | |
Myasthenia gravis | Accepted[7] | II | nicotinic acetylcholine receptor MuSK protein | HA-B8 HLA-DR3 HLA-DR1 | |
Microscopic colitis | Suspected | ||||
Myositis | see Dermatomyositis and Polymyositis see Inclusion-body-myositis | ||||
Narcolepsy[51][52] | Accepted | II? | hypocretin or orexin[53] | HLA-DQB1*0602[54] | |
Neuromyelitis optica (also Devic's disease) | II? | NMO-IgG aquaporin 4.[55][56] | |||
Neuromyotonia | Suspected[57] | II? | voltage-gated potassium channels.[57] | ||
Occular cicatricial pemphigoid | II? | BP-1, BP-2 | C3 deposition | ||
Opsoclonus myoclonus syndrome | Suspected | IV? | Lymphocyte recruitment to CSF[58] | ||
Ord's thyroiditis | |||||
Palindromic rheumatism | anti-cyclic citrullinated peptide antibodies (anti-CCP) and antikeratin antibodies (AKA)[59] | ||||
PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcus) | Suspected | II? | antibodies against streptococcal infection serve as auto-antibodies | ||
Paraneoplastic cerebellar degeneration | IV?[60] II? | anti-Yo[61] (anti-cdr-2[62] in purkinje fibers) anti-Hu, anti-Tr, antiglutamate receptor | |||
Paroxysmal nocturnal hemoglobinuria (PNH) | Sometimes(?) | complement attacks RBCs | |||
Parry Romberg syndrome | ANA | ||||
Parsonage-Turner syndrome | |||||
Pars planitis | |||||
Pemphigus vulgaris | Accepted[7] | II | Anti-Desmoglein 3 eosinophilia[21] | ||
Pernicious anaemia | Accepted[63] | II | anti-parietal cell antibody | ||
Perivenous encephalomyelitis | |||||
POEMS syndrome | interleukin 1β, interleukin 6 and TNFα. vascular endothelial growth factor (VEGF), given the .[64] | ||||
Polyarteritis nodosa | |||||
Polymyalgia rheumatica | |||||
Polymyositis | Accepted[24] | IFN-gamma, IL-1, TNF-alpha | |||
Primary biliary cirrhosis | Accepted[65] | Anti-p62, Anti-sp100, Anti-Mitochondrial(M2)Anti-Ro aka SSA.[44] Also, they are often present in Sjögren's syndrome.[45][46] | |||
Primary sclerosing cholangitis | HLA-DR52a | overlap with primary biliary cirrhosis? | |||
Progressive inflammatory neuropathy | Suspected | ||||
Psoriasis | Accepted[66] | IV? | CD-8 T-cells, HLA-Cw6, IL-12b, IL-23b, TNFalpha, NF-κB | ||
Psoriatic arthritis | Accepted[67] | IV? | HLA-B27 | ||
Pyoderma gangrenosum | Can occur in conjunction with other immune-related disorders | ||||
Pure red cell aplasia | |||||
Rasmussen's encephalitis | anti-NR2A antibodies | ||||
Raynaud phenomenon | Suspected | Can occur in conjunction with other immune-related disorders | |||
Relapsing polychondritis | Accepted[68] | ||||
Reiter's syndrome | |||||
Restless leg syndrome | Suspected | May occur in Sjögren's syndrome, celiac disease, and rheumatoid arthritis or in derangements of iron metabolism | |||
Retroperitoneal fibrosis | |||||
Rheumatoid arthritis | Accepted[7] | III | Rheumatoid factor (anti-IgGFc), Anti-MCV, ACPAs(Vimentin | HLA-DR4, PTPN22, depleted B cells, TNF alpha, IL-17, (also maybe IL-1, 6, and 15) | |
Rheumatic fever | Accepted[69] | II | streptococcal M protein cross reacts with human myosin,[70] | ||
Sarcoidosis | Suspected | IV[71][72] | BTNL2; HLA-B7-DR15; HLA DR3-DQ2.[73] | ||
Schizophrenia | Suspected[74][75][76] | ||||
Schmidt syndrome another form of APS | anti-21 hydroxylase, anti-17 hydroxylase[77] | DQ2, DQ8 and DRB1*0404 | |||
Schnitzler syndrome | IgM? | ||||
Scleritis | |||||
Scleroderma | Suspected[48] | IV? | Scl-70 Anti-topoisomerase | dysregulated apoptosis? | |
Serum Sickness | III | ||||
Sjögren's syndrome | Accepted[7] | anti-Ro.[44] Also, they are often present in Sjögren's syndrome.[45][46] | |||
Spondyloarthropathy | HLA-B27 | ||||
Still's disease see Juvenile Rheumatoid Arthritis | ANA | macrophage migration inhibitory factor[78] | |||
Stiff person syndrome | Suspected | glutamic acid decarboxylase (GAD),[79] | GLRA1 (glycine receptor) | ||
Subacute bacterial endocarditis (SBE) | III [80] | essential mixed cryoglobulinemia | |||
Susac's syndrome | |||||
Sweet's syndrome | GCSF | ||||
Sydenham chorea see PANDAS | |||||
Sympathetic ophthalmia | ocular antigens following trauma | ||||
Systemic lupus erythematosus see Lupus erythematosus | III | ||||
Takayasu's arteritis | |||||
Temporal arteritis (also known as "giant cell arteritis") | Accepted[7] | IV | |||
Thrombocytopenia | II | glycoproteins IIb-IIIa or Ib-IX in ITP anti-ADAMTS13 in TTP.[81] and HUS anti-cardiolipin (anti-cardiolipin antibodies) and β2 glycoprotein I in Antiphospholipid syndrome anti-HPA-1a, anti-HPA-5b, and others[82] in NAIT | multiple mechanisms | ||
Tolosa-Hunt syndrome | |||||
Transverse myelitis | Accepted | Transverse Myelitis is a rare neurological disorder that is part of a spectrum of neuroimmunologic diseases of the central nervous system. http://www.myelitis.org/ | |||
Ulcerative colitis (one of two types of idiopathic inflammatory bowel disease "IBD") | Accepted[7] | IV | |||
Undifferentiated connective tissue disease different from Mixed connective tissue disease | Accepted | anti-nuclear antibody | HLA-DR4 | ||
Undifferentiated spondyloarthropathy | |||||
Urticarial vasculitis | II? | anti C1q antibodies[83] | clinically may resemble type I hypersensitivity! | ||
Vasculitis | Accepted[14] | III | sometimes ANCA | ||
Vitiligo | Suspected[84][85] | NALP-1 RERE, PTPN22, LPP, IL2RA, GZMB, UBASH3A and C1QTNF6 | |||
Wegener's granulomatosis | Accepted[86] | Anti-neutrophil cytoplasmic(cANCA) |
Development of therapies
In both autoimmune and inflammatory diseases, the condition arises through aberrant reactions of the human adaptive or innate immune systems. In autoimmunity, the patient’s immune system is activated against the body's own proteins. In chronic inflammatory diseases, neutrophils and other leukocytes are constitutively recruited by cytokines and chemokines, leading to tissue damage.
Mitigation of inflammation by activation of anti-inflammatory genes and the suppression of inflammatory genes in immune cells is a promising therapeutic approach.[87][88][89]
See also
- Autoimmunity
- Immune-mediated disease
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- ^ Hallmayer J, Faraco J, Lin L, Hesselson S, Winkelmann J, Kawashima M, Mayer G, Plazzi G, Nevsimalova S, Bourgin P, Hong SC, Hong SS, Honda Y, Honda M, Högl B, Longstreth WT, Montplaisir J, Kemlink D, Einen M, Chen J, Musone SL, Akana M, Miyagawa T, Duan J, Desautels A, Erhardt C, Hesla PE, Poli F, Frauscher B, Jeong JH, Lee SP, Ton TG, Kvale M, Kolesar L, Dobrovolná M, Nepom GT, Salomon D, Wichmann HE, Rouleau GA, Gieger C, Levinson DF, Gejman PV, Meitinger T, Young T, Peppard P, Tokunaga K, Kwok PY, Risch N, Mignot E (June 2009). "Narcolepsy is strongly associated with the TCR alpha locus". Nat. Genet. 41 (6): 708–11. doi:10.1038/ng.372. PMC 2803042. PMID 19412176.
- ^ "Narcolepsy is an autoimmune disorder, Stanford researcher says". EurekAlert. American Association for the Advancement of Science. 2009-05-03. Archived from the original on 10 May 2009. Retrieved 2009-05-31.
- ^ Mignot E (2001). "A commentary on the neurobiology of the hypocretin/orexin system". Neuropsychopharmacology 25 (5 Suppl): S5–13. doi:10.1016/S0893-133X(01)00316-5. PMID 11682267.
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- ^ Lennon VA, Kryzer TJ, Pittock SJ, Verkman AS, Hinson SR (2005). "IgG marker of optic-spinal multiple sclerosis binds to the aquaporin-4 water channel". J. Exp. Med. 202 (4): 473–477. doi:10.1084/jem.20050304. PMC 2212860. PMID 16087714.
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- ^ Powell A, Davis P, Jones N, Russell AS (June 2008). "Palindromic rheumatism is a common disease: comparison of new-onset palindromic rheumatism compared to new-onset rheumatoid arthritis in a 2-year cohort of patients". J. Rheumatol. 35 (6): 992–4. PMID 18412310.
- ^ Darnell,R.B. (1996), "Onconeural antigens and the paraneoplastic neurologic disorders: at the intersection of cancer, immunity, and the brain", Proceedings of the National Academy of Sciences of the United States of America 93 (10): 4529–4536, doi:10.1073/pnas.93.10.4529, PMC 39311, PMID 8643438
- ^ Peterson K, Rosenblum MK, Kotanides H, Posner JB (1992). "Paraneoplastic cerebellar degeneration. I. A clinical analysis of 55 anti-Yo antibody-positive patients". Neurology 42 (10): 1931–7. PMID 1407575.
- ^ Albert ML, Austin LM, Darnell RB (2000). "Detection and treatment of activated T cells in the cerebrospinal fluid of patients with paraneoplastic cerebellar degeneration". Annals of Neurology 47 (1): 9–17. doi:10.1002/1531-8249(200001)47:1<9::aid-ana5>3.3.co;2-9. PMID 10632096.
- ^ "MedlinePlus Medical Encyclopedia: Pernicious anemia". Archived from the original on 9 May 2008. Retrieved 2008-04-05.
- ^ Dispenzieri A, Kyle RA, Lacy MQ, Rajkumar SV, Therneau TM, Larson DR, Greipp PR, Witzig TE, Basu R, Suarez GA, Fonseca R, Lust JA, Gertz MA (2003). "POEMS syndrome: definitions and long-term outcome". Blood 101 (7): 2496–506. doi:10.1182/blood-2002-07-2299. PMID 12456500.
- ^ "Primary Biliary Cirrhosis: Fatty Liver, Cirrhosis, and Related Disorders: Merck Manual Home Health Handbook". Retrieved 2008-04-05.
- ^ National Psoriasis Foundation, http://www.psoriasis.org/home/learn01.php
- ^ National Psoriasis Foundation, http://www.psoriasis.org/home/learn02.php
- ^ "Relapsing Polychondritis: Autoimmune Disorders of Connective Tissue: Merck Manual Home Health Handbook".
- ^ Girschick HJ, Guilherme L, Inman RD, Latsch K, Rihl M, Sherer Y, Shoenfeld Y, Zeidler H, Arienti S, Doria A (2008). "Bacterial triggers and autoimmune rheumatic diseases". Clinical and Experimental Rheumatology 26 (1 Suppl 48): S12–7. PMID 18570749.
- ^ Faé KC, da Silva DD, Oshiro SE, Tanaka AC, Pomerantzeff PM, Douay C, Charron D, Toubert A, Cunningham MW, Kalil J, Guilherme L (May 2006). "Mimicry in recognition of cardiac myosin peptides by heart-intralesional T cell clones from rheumatic heart disease". J. Immunol. 176 (9): 5662–70. doi:10.4049/jimmunol.176.9.5662. PMID 16622036.
- ^ "eMedicine - Hypersensitivity Reactions, Delayed : Article by Walter Duane Hinshaw". Archived from the original on 15 September 2008. Retrieved 2008-09-18.
- ^ Morell F, Levy G, Orriols R, Ferrer J, De Gracia J, Sampol G (April 2002). "Delayed cutaneous hypersensitivity tests and lymphopenia as activity markers in sarcoidosis". Chest 121 (4): 1239–44. doi:10.1378/chest.121.4.1239. PMID 11948059.
- ^ Grunewald J, Eklund A, Olerup O (March 2004). "Human leukocyte antigen class I alleles and the disease course in sarcoidosis patients". Am. J. Respir. Crit. Care Med. 169 (6): 696–702. doi:10.1164/rccm.200303-459OC. PMID 14656748.
- ^ Eaton WW, Byrne M, Ewald H, Mors O, Chen CY, Agerbo E, Mortensen PB (2006). "Association of schizophrenia and autoimmune diseases: linkage of Danish national registers". The American Journal of Psychiatry 163 (3): 521–8. doi:10.1176/appi.ajp.163.3.521. PMID 16513876.
- ^ Jones AL, Mowry BJ, Pender MP, Greer JM (2005). "Immune dysregulation and self-reactivity in schizophrenia: do some cases of schizophrenia have an autoimmune basis?". Immunol. Cell Biol. 83 (1): 9–17. doi:10.1111/j.1440-1711.2005.01305.x. PMID 15661036.
- ^ Strous RD, Shoenfeld Y (2006). "Schizophrenia, autoimmunity and immune system dysregulation: a comprehensive model updated and revisited". J. Autoimmun. 27 (2): 71–80. doi:10.1016/j.jaut.2006.07.006. PMID 16997531.
- ^ de Carmo Silva R, Kater CE, Dib SA, Laureti S, Forini F, Cosentino A, Falorni A (February 2000). "Autoantibodies against recombinant human steroidogenic enzymes 21-hydroxylase, side-chain cleavage and 17alpha-hydroxylase in Addison's disease and autoimmune polyendocrine syndrome type III". Eur. J. Endocrinol. 142 (2): 187–94. doi:10.1530/eje.0.1420187. PMID 10664529. Retrieved 2008-07-25.
- ^ De Benedetti F, Meazza C, Vivarelli M, Rossi F, Pistorio A, Lamb R, Lunt M, Thomson W, Ravelli A, Donn R, Martini A (May 2003). "Functional and prognostic relevance of the -173 polymorphism of the macrophage migration inhibitory factor gene in systemic-onset juvenile idiopathic arthritis". Arthritis Rheum. 48 (5): 1398–407. doi:10.1002/art.10882. PMID 12746913.
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- ^ Mueller-Eckhardt C, Kiefel V, Grubert A, Kroll H, Weisheit M, Schmidt S, Mueller-Eckhardt G, Santoso S (1989). "348 cases of fetal alloimmune thrombocytopenia". Lancet 1 (8634): 363–6. doi:10.1016/S0140-6736(89)91733-9. PMID 2563515.
- ^ Wisnieski JJ, Naff GB (September 1989). "Serum IgG antibodies to C1q in hypocomplementemic urticarial vasculitis syndrome". Arthritis Rheum 32 (9): 1119–27. doi:10.1002/anr.1780320910. PMID 2528353.
- ^ "Questions and Answers about Vitiligo". Retrieved 2007-08-06.
- ^ "A New Gene Linked to Vitiligo and Susceptibility to Autoimmune Disorders - Journal Watch Dermatology". Archived from the original on 3 September 2007. Retrieved 2007-08-06.
- ^ Sánchez-Cano D, Callejas-Rubio JL, Ortego-Centeno N (April 2008). "Effect of rituximab on refractory Wegener granulomatosis with predominant granulomatous disease". J Clin Rheumatol 14 (2): 92–3. doi:10.1097/RHU.0b013e31816b4487. PMID 18391678.
- ^ Mukundan L, Odegaard JI, Morel CR, Heredia JE, Mwangi JW, Ricardo-Gonzalez RR, Goh YP, Eagle AR, Dunn SE et al. (Nov 2009). "PPAR-delta senses and orchestrates clearance of apoptotic cells to promote tolerance". Nat Med 15 (11): 1266–72. doi:10.1038/nm.2048.
- ^ Roszer T, Menéndez-Gutiérrez MP, Lefterova MI, Alameda D, Núñez V, Lazar MA, Fischer T, Ricote M (Jan 2011). "Autoimmune kidney disease and impaired engulfment of apoptotic cells in mice with macrophage peroxisome proliferator-activated receptor gamma or retinoid X receptor alpha deficiency". J Immunol 186 (1): 621–31. doi:10.4049/jimmunol.1002230.
- ^ Singh RP, Waldron RT, Hahn BH (2012). "Genes, tolerance and systemic autoimmunity". Autoimmunity Reviews 11 (9): 664–9. doi:10.1016/j.autrev.2011.11.017. PMC 3306516. PMID 22155015.
Further reading
- Vinay Kumar, Abul K. Abbas, Nelson Fausto, Jon Aster, Robbins and Cotran Pathologic Basis of Disease, Elsevier, 8th edition, 2010, 1464 pp., ISBN 978-1-4160-3121-5
- Handbook of Systemic Autoimmune Diseases, edited by Ronald Asherson, Elsevier, in 10 Volumes: http://www.elsevier.com/wps/find/bookdescription.cws_home/BS_HSAD/description#description
- Ronald Asherson, Andrea Doria, Paolo Pauletto, The Heart in Systemic Autoimmune Diseases, Volume 1, 2004, ISBN 978-0-444-51398-4, ISBN 0-444-51398-1
- Ronald Asherson, Andrea Doria, Paolo Pauletto, Pulmonary Involvement in Systemic Autoimmune Diseases, Volume 2, 2005, ISBN 978-0-444-51652-7, ISBN 0-444-51652-2
- Ronald Asherson, Doruk Erkan, Steven Levine, The Neurologic Involvement in Systemic Autoimmune Diseases, Volume 3, 2005, ISBN 978-0-444-51651-0, ISBN 0-444-51651-4
- Michael Lockshin, Ware Branch (eds), Reproductive and Hormonal Aspects of Systemic Autoimmune Diseases, Volume 4, 2006, ISBN 978-0-444-51801-9, ISBN 0-444-51801-0
- Piercarlo Sarzi-Puttini, Ronald Asherson, Andrea Doria, Annegret Kuhn, Giampietro Girolomoni (eds), The Skin in Systemic Autoimmune Diseases, Volume Volume 5, 2006, ISBN 978-0-444-52158-3, ISBN 0-444-52158-5
- Rolando Cimaz, Ronald Asherson, Thomas Lehman (eds), Pediatrics in Systemic Autoimmune Diseases, Volume 6, 2008, ISBN 978-0-444-52971-8, ISBN 0-444-52971-3
- Justin Mason, Ronald Asherson, Charles Pusey (eds), The Kidney in Systemic Autoimmune Diseases, Volume 7, 2008, ISBN 978-0-444-52972-5, ISBN 0-444-52972-1
- Ronald Asherson, Manel Ramos-Casals, Joan Rodes, Josep Font, Digestive Involvement in Systemic Autoimmune Diseases, Volume 8, 2008, ISBN 978-0-444-53168-1, ISBN 0-444-53168-8
- Ronald Asherson, Sara Walker, Luis Jara, Endocrine Manifestations of Systemic Autoimmune Diseases, Volume 9, 2008, ISBN 978-0-444-53172-8, ISBN 0-444-53172-6
- R. Cervera, Ronald Asherson, Munther Khamashta, Joan Carles Reverter (eds), Antiphospholipid Syndrome in Systemic Autoimmune Diseases, Volume 10, 2009, ISBN 978-0-444-53169-8, ISBN 0-444-53169-6
- www.autoimmunityblog.com - a glossary of autoimmune diseases and the related autoantibodies plus summaries of recent research articles.
External links
- Auto-immune disorders at DMOZ
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Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2017/07/21 21:19:55」(JST)
wiki en
[Wiki en表示]Autoimmune diseases | |
---|---|
Young woman with the typical "butterfly rash" found in lupus | |
Specialty | Rheumatology, immunology, gastroenterology, other |
Symptoms | Depends on the condition. Commonly low grade fever, feeling tired[1] |
Usual onset | Adulthood[1] |
Types | Alopecia areata, Celiac disease, diabetes mellitus type 1, Graves disease, inflammatory bowel disease, multiple sclerosis, psoriasis, rheumatoid arthritis, systemic lupus erythematosus[1] |
Medication | Nonsteroidal anti-inflammatory drugs, immunosuppressants, intravenous Immunoglobulin[1][2] |
Frequency | 24 million / 7% (USA)[1][3] |
[edit on Wikidata]
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An autoimmune disease is a condition arising from an abnormal immune response to a normal body part.[1] There are at least 80 types of autoimmune diseases.[1] Nearly any body part can be involved.[3] Common symptoms include low grade fever and feeling tired. Often symptoms come and go.[1]
The cause is generally unknown.[3] Some autoimmune diseases such as lupus run in families, and certain cases may be triggered by infections or other environmental factors. Some common autoimmune disease include celiac disease, diabetes mellitus type 1, Graves disease, inflammatory bowel disease, multiple sclerosis, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus. The diagnosis can be difficult to determine.[1]
Treatment depends on the type and severity of the condition. Nonsteroidal anti-inflammatory drugs (NSAIDs) and immunosuppressants are often used.[1] Intravenous Immunoglobulin may also occasionally be used.[2] While treatment usually improves symptoms they do not typically cure the disease.[1]
About 24 million (7%) people in the United States are affected by an autoimmune disease.[1][3] Women are more commonly affected than men. Often they start during adulthood.[1] The first autoimmune diseases were described in the early 1900s.[4]
Contents
- 1 Definition
- 2 Signs and symptoms
- 3 Pathophysiology
- 3.1 Cryptic determinants/molecular sequestration
- 3.2 Molecular mimicry
- 3.3 Altered glycan theory
- 3.4 Hygiene hypothesis
- 4 Epidemiology
- 5 Research
- 6 History
- 7 References
- 8 Further reading
- 9 External links
Definition
For a disease to be regarded as an autoimmune disease it needs to answer to Witebsky's postulates (first formulated by Ernest Witebsky and colleagues in 1957 and modified in 1994):[5][6]
- Direct evidence from transfer of disease-causing antibody or disease-causing T lymphocyte white blood cells
- Indirect evidence based on reproduction of the autoimmune disease in experimental animals
- Circumstantial evidence from clinical clues
- Genetic evidence suggesting "clustering" with other autoimmune diseases
- Autoimmune diseases are incurable
Signs and symptoms
Autoimmune diseases have a wide variety of different effects. They do tend to have one of three characteristic pathological effects which characterize them as autoimmune diseases:[7]
- Damage to or destruction of tissues
- Altered organ growth
- Altered organ function
It has been estimated that autoimmune diseases are among the leading causes of death among women in the United States in all age groups up to 65 years.[8]
A substantial minority of the population suffers from these diseases, which are often chronic, debilitating, and life-threatening.[citation needed]
There are more than 80 illnesses caused by autoimmunity.[9] Autoimmune diseases affect approximately 2-5% of the western world's population. Women are found to be more commonly affected than men. Environmental events can trigger some cases of autoimmune diseases such as exposure to radiation or certain drugs which can damage tissues of the body. Infection can also be a trigger of some autoimmune diseases for example Lupus which is thought to be a milder version of an idiopathic disorder where there is an increased production of antihistone antibodies.[7]
Pathophysiology
The human immune system typically produces both T-cells and B-cells that are capable of being reactive with self-antigens, but these self-reactive cells are usually either killed prior to becoming active within the immune system, placed into a state of anergy (silently removed from their role within the immune system due to over-activation), or removed from their role within the immune system by regulatory cells. When any one of these mechanisms fail, it is possible to have a reservoir of self-reactive cells that become functional within the immune system. The mechanisms of preventing self-reactive T-cells from being created takes place through negative selection process within the thymus as the T-cell is developing into a mature immune cell.
Some infections, such as Campylobacter jejuni, have antigens that are similar (but not identical) to our own self-molecules. In this case, a normal immune response to C. jejuni can result in the production of antibodies that also react to a lesser degree with receptors on skeletal muscle (i.e., Myasthenia gravis). A major understanding of the underlying pathophysiology of autoimmune diseases has been the application of genome wide association scans that have identified a degree of genetic sharing among the autoimmune diseases.[10]
Autoimmunity, on the other hand, is the presence of self-reactive immune response (e.g., auto-antibodies, self-reactive T-cells), with or without damage or pathology resulting from it.[11] This may be restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue in different places (e.g. Goodpasture's disease which may affect the basement membrane in both the lung and the kidney).
There are many theories as to how an autoimmune disease state arises. Some common ones are listed below.
Cryptic determinants/molecular sequestration
Although it is possible for a potential autoantigen to be geographically sequestered in an immune privileged site within the body (e.g. the eye), mechanisms exist to express even these antigens in a tolerogenic fashion to the immune system. However, it is impossible to induce tolerance (immune unresponsiveness) to all aspects of an autoantigen. This is because under normal physiologic conditions some regions of a self-antigen are not expressed at a sufficient level to induce tolerance. These poorly displayed areas of an antigen are called "cryptic determinants." The immune system maintains a high-affinity repertoire to the cryptic self because the presentation of these determinants was insufficient to induce strong tolerance.[12]
Molecular mimicry
The concept of molecular mimicry describes a situation in which a foreign antigen can initiate an immune response in which a T or B cell component cross-recognizes self. The cross reactive immune response is responsible for the autoimmune disease state.[13] Cross-reactive immune responses to self were first described for antibodies.
Altered glycan theory
According to this theory the effector function of the immune response is mediated by the glycans (polysaccharides) displayed by the cells and humoral components of the immune system. Individuals with autoimmunity have alterations in their glycosylation profile such that a proinflammatory immune response is favored. It is further hypothesized that individual autoimmune diseases will have unique glycan signatures.[14]
Hygiene hypothesis
According to the hygiene hypothesis, high levels of cleanliness expose children to fewer antigens than in the past, causing their immune systems to become overactive and more likely to misidentify own tissues as foreign, resulting in autoimmune conditions such as asthma.[15]
Epidemiology
The first estimate of US prevalence for autoimmune diseases as a group was published in 1997 by Jacobson, et al. They reported US prevalence to be around 9 million, applying prevalence estimates for 24 diseases to a US population of 279 million.[16] Jacobson's work was updated by Hayter & Cook in 2012.[17] This study used Witebsky's postulates, as revised by Rose & Bona,[18] to extend the list to 81 diseases and estimated overall cumulative US prevalence for the 81 autoimmune diseases at 5.0%, with 3.0% for males and 7.1% for females. The estimated community prevalence, which takes into account the observation that many people have more than one autoimmune disease, was 4.5% overall, with 2.7% for males and 6.4% for females.[17]
Research
In both autoimmune and inflammatory diseases, the condition arises through aberrant reactions of the human adaptive or innate immune systems. In autoimmunity, the patient's immune system is activated against the body's own proteins. In chronic inflammatory diseases, neutrophils and other leukocytes are constitutively recruited by cytokines and chemokines, leading to tissue damage.
Mitigation of inflammation by activation of anti-inflammatory genes and the suppression of inflammatory genes in immune cells is a promising therapeutic approach.[19][20][21] There is a body of evidence that once the production of autoantibodies has been initialized, autoantibodies have the capacity to maintain their own production.[22]
Stem cell transplantation is being studied and has shown promising results in certain cases.[23]
History
Traditionally it was believed that the immune system was unable to react against the body's own tissues, a concept described by the German immunologist Paul Ehrlich as "horror autotoxicus". In 1904 this theory was challenged by the discovery of a substance in the serum of patients with paroxysmal cold hemoglobinuria that reacted with red blood cells.[24]
References
- ^ a b c d e f g h i j k l m "Autoimmune diseases fact sheet". OWH. 16 July 2012. Retrieved 5 October 2016.
- ^ a b Katz, U; Shoenfeld, Y; Zandman-Goddard, G (2011). "Update on intravenous immunoglobulins (IVIg) mechanisms of action and off- label use in autoimmune diseases.". Current pharmaceutical design. 17 (29): 3166–75. PMID 21864262. doi:10.2174/138161211798157540.
- ^ a b c d Borgelt, Laura Marie (2010). Women's Health Across the Lifespan: A Pharmacotherapeutic Approach. ASHP. p. 579. ISBN 9781585281947.
- ^ Paniker, Ananthanarayan And (169). Ananthanarayan and Paniker's Textbook of Microbiology. 2005: Orient Blackswan. ISBN 9788125028086.
- ^ Witebsky E, Rose NR, Terplan K, Paine JR, Egan RW (1957). "Chronic thyroiditis and autoimmunization". J. Am. Med. Assoc. 164 (13): 1439–47. PMID 13448890. doi:10.1001/jama.1957.02980130015004.
- ^ Rose NR, Bona C (September 1993). "Defining criteria for autoimmune diseases (Witebsky's postulates revisited)". Immunol. Today. 14 (9): 426–30. PMID 8216719. doi:10.1016/0167-5699(93)90244-F.
- ^ "Autoimmune disorders: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2016-01-21.
- ^ Walsh, SJ; Rau, LM (September 2000). "Autoimmune diseases: a leading cause of death among young and middle-aged women in the United States.". American Journal of Public Health. 90 (9): 1463–6. PMC 1447637 . PMID 10983209. doi:10.2105/ajph.90.9.1463.
- ^ "MedlinePlus medical encyclopedia - autoimmune disorders". National Institutes of Health. 16 July 2014. Retrieved 21 December 2014.
- ^ Cotsapas C, Hafler DA (2013). "Immune-mediated disease genetics: the shared basis of pathogenesis". Trends in Immunology. 34 (1): 22–6. PMID 23031829. doi:10.1016/j.it.2012.09.001.
- ^ Harrison's Principles of Internal Medicine: Volumes 1 and 2, 18th Edition (18 ed.). McGraw-Hill Professional. 2011-08-11. ISBN 9780071748896.
- ^ Gammon G, Sercarz E (1989). "How some T cells escape tolerance induction". Nature. 342: 6246. PMID 2478888. doi:10.1038/342183a0.
- ^ Wucherpfennig KW, Strominger JL (1995). "Molecular mimicry in T cell-mediated autoimmunity: viral peptides activate human T cell clones specific for myelin basic protein.". Cell. 80 (5): 695–705. PMID 7534214. doi:10.1016/0092-8674(95)90348-8.
- ^ Maverakis E, Kim K, Shimoda M, Gershwin M, Patel F, Wilken R, Raychaudhuri S, Ruhaak LR, Lebrilla CB (2015). "Glycans in the immune system and The Altered Glycan Theory of Autoimmunity". J Autoimmun. 57 (6): 1–13. PMC 4340844 . PMID 25578468. doi:10.1016/j.jaut.2014.12.002.
- ^ Rook, Graham A. W. (17 November 2011). "Hygiene Hypothesis and Autoimmune Diseases". Clinical Reviews in Allergy & Immunology. 42 (1): 5–15. PMID 22090147. doi:10.1007%2Fs12016-011-8285-8 Check
|doi=
value (help). - ^ Jacobson, DL; Gange, SJ; Rose, NR; Graham, NM (September 1997). "Epidemiology and estimated population burden of selected autoimmune diseases in the United States.". Clinical immunology and immunopathology. 84 (3): 223–43. PMID 9281381. doi:10.1006/clin.1997.4412.
- ^ a b Hayter, SM; Cook, MC (August 2012). "Updated assessment of the prevalence, spectrum and case definition of autoimmune disease.". Autoimmunity reviews. 11 (10): 754–65. PMID 22387972. doi:10.1016/j.autrev.2012.02.001.
- ^ Rose, NR; Bona, C (September 1993). "Defining criteria for autoimmune diseases (Witebsky's postulates revisited)". Immunology today. 14 (9): 426–30. PMID 8216719. doi:10.1016/0167-5699(93)90244-F.
- ^ Mukundan L, Odegaard JI, Morel CR, Heredia JE, Mwangi JW, Ricardo-Gonzalez RR, Goh YP, Eagle AR, Dunn SE, et al. (Nov 2009). "PPAR-delta senses and orchestrates clearance of apoptotic cells to promote tolerance". Nat Med. 15 (11): 1266–72. PMC 2783696 . PMID 19838202. doi:10.1038/nm.2048.
- ^ Roszer T, Menéndez-Gutiérrez MP, Lefterova MI, Alameda D, Núñez V, Lazar MA, Fischer T, Ricote M (Jan 2011). "Autoimmune kidney disease and impaired engulfment of apoptotic cells in mice with macrophage peroxisome proliferator-activated receptor gamma or retinoid X receptor alpha deficiency". J Immunol. 186 (1): 621–31. PMID 21135166. doi:10.4049/jimmunol.1002230.
- ^ Singh RP, Waldron RT, Hahn BH (2012). "Genes, tolerance and systemic autoimmunity". Autoimmunity Reviews. 11 (9): 664–9. PMC 3306516 . PMID 22155015. doi:10.1016/j.autrev.2011.11.017.
- ^ Böhm I (2003). "Disruption of the cytoskeleton after apoptosis induction by autoantibodies". Autoimmunity. 36 (3): 183–9. PMID 12911286.
- ^ Swart, JF; Delemarre, EM; van Wijk, F; Boelens, JJ; Kuball, J; van Laar, JM; Wulffraat, NM (April 2017). "Haematopoietic stem cell transplantation for autoimmune diseases.". Nature reviews. Rheumatology. 13 (4): 244–256. PMID 28228650.
- ^ Moticka, Edward J. (2013). Historical perspective on evidence-based immunology. Elsevier Science Publishing. p. 300. ISBN 9780123983817.
Further reading
- Vinay Kumar, Abul K. Abbas, Nelson Fausto, Jon Aster, Robbins and Cotran Pathologic Basis of Disease, Elsevier, 8th edition, 2010, 1464 pp., ISBN 978-1-4160-3121-5
- Handbook of Systemic Autoimmune Diseases, edited by Ronald Asherson, Elsevier, in 10 Volumes: http://www.elsevier.com/wps/find/bookdescription.cws_home/BS_HSAD/description#description
- Ronald Asherson, Andrea Doria, Paolo Pauletto, The Heart in Systemic Autoimmune Diseases, Volume 1, 2004, ISBN 978-0-444-51398-4, ISBN 0-444-51398-1
- Ronald Asherson, Andrea Doria, Paolo Pauletto, Pulmonary Involvement in Systemic Autoimmune Diseases, Volume 2, 2005, ISBN 978-0-444-51652-7, ISBN 0-444-51652-2
- Ronald Asherson, Doruk Erkan, Steven Levine, The Neurologic Involvement in Systemic Autoimmune Diseases, Volume 3, 2005, ISBN 978-0-444-51651-0, ISBN 0-444-51651-4
- Michael Lockshin, Ware Branch (eds), Reproductive and Hormonal Aspects of Systemic Autoimmune Diseases, Volume 4, 2006, ISBN 978-0-444-51801-9, ISBN 0-444-51801-0
- Piercarlo Sarzi-Puttini, Ronald Asherson, Andrea Doria, Annegret Kuhn, Giampietro Girolomoni (eds), The Skin in Systemic Autoimmune Diseases, Volume Volume 5, 2006, ISBN 978-0-444-52158-3, ISBN 0-444-52158-5
- Rolando Cimaz, Ronald Asherson, Thomas Lehman (eds), Pediatrics in Systemic Autoimmune Diseases, Volume 6, 2008, ISBN 978-0-444-52971-8, ISBN 0-444-52971-3
- Justin Mason, Ronald Asherson, Charles Pusey (eds), The Kidney in Systemic Autoimmune Diseases, Volume 7, 2008, ISBN 978-0-444-52972-5, ISBN 0-444-52972-1
- Ronald Asherson, Manel Ramos-Casals, Joan Rodes, Josep Font, Digestive Involvement in Systemic Autoimmune Diseases, Volume 8, 2008, ISBN 978-0-444-53168-1, ISBN 0-444-53168-8
- Ronald Asherson, Sara Walker, Luis Jara, Endocrine Manifestations of Systemic Autoimmune Diseases, Volume 9, 2008, ISBN 978-0-444-53172-8, ISBN 0-444-53172-6
- R. Cervera, Ronald Asherson, Munther Khamashta, Joan Carles Reverter (eds), Antiphospholipid Syndrome in Systemic Autoimmune Diseases, Volume 10, 2009, ISBN 978-0-444-53169-8, ISBN 0-444-53169-6
External links
Classification |
|
---|---|
External resources |
|
- Autoimmune disorders at DMOZ
Hypersensitivity and autoimmune diseases (279.5–6)
|
|||||||||
---|---|---|---|---|---|---|---|---|---|
Type I/allergy/atopy (IgE) |
|
||||||||
Type II/ADCC
|
|
||||||||
Type III (Immune complex) |
|
||||||||
Type IV/cell-mediated (T cells) |
|
||||||||
Unknown/ multiple |
|
- Biology portal
- Medicine portal
Authority control |
|
---|
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2018/01/16 08:43:59」(JST)
wiki en
[Wiki en表示]Autoimmune diseases | |
---|---|
Young woman with the typical "butterfly rash" found in lupus | |
Specialty | Rheumatology, immunology, gastroenterology, other |
Symptoms | Depends on the condition. Commonly low grade fever, feeling tired[1] |
Usual onset | Adulthood[1] |
Types | Alopecia areata, Celiac disease, diabetes mellitus type 1, Graves disease, inflammatory bowel disease, multiple sclerosis, psoriasis, rheumatoid arthritis, systemic lupus erythematosus[1] |
Medication | Nonsteroidal anti-inflammatory drugs, immunosuppressants, intravenous Immunoglobulin[1][2] |
Frequency | 24 million / 7% (USA)[1][3] |
[edit on Wikidata]
|
An autoimmune disease is a condition arising from an abnormal immune response to a normal body part.[1] There are at least 80 types of autoimmune diseases.[1] Nearly any body part can be involved.[3] Common symptoms include low grade fever and feeling tired.[1] Often symptoms come and go.[1]
The cause is generally unknown.[3] Some autoimmune diseases such as lupus run in families, and certain cases may be triggered by infections or other environmental factors.[1] Some common diseases that are generally considered autoimmune include celiac disease, diabetes mellitus type 1, Graves' disease, inflammatory bowel disease, multiple sclerosis, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus.[1][4] The diagnosis can be difficult to determine.[1]
Treatment depends on the type and severity of the condition.[1] Nonsteroidal anti-inflammatory drugs (NSAIDs) and immunosuppressants are often used.[1] Intravenous Immunoglobulin may also occasionally be used.[2] While treatment usually improves symptoms they do not typically cure the disease.[1]
About 24 million (7%) people in the United States are affected by an autoimmune disease.[1][3] Women are more commonly affected than men.[1] Often they start during adulthood.[1] The first autoimmune diseases were described in the early 1900s.[5]
Contents
- 1 Definition
- 2 Signs and symptoms
- 3 Pathophysiology
- 3.1 Cryptic determinants/molecular sequestration
- 3.2 Molecular mimicry
- 3.3 Altered glycan theory
- 3.4 Hygiene hypothesis
- 4 Epidemiology
- 5 Research
- 6 History
- 7 References
- 8 Further reading
- 9 External links
Definition
For a disease to be regarded as an autoimmune disease it needs to answer to Witebsky's postulates (first formulated by Ernest Witebsky and colleagues in 1957 and modified in 1994):[6][7]
- Direct evidence from transfer of disease-causing antibody or disease-causing T lymphocyte white blood cells
- Indirect evidence based on reproduction of the autoimmune disease in experimental animals
- Circumstantial evidence from clinical clues
- Genetic evidence suggesting "clustering" with other autoimmune diseases
Signs and symptoms
Autoimmune diseases have a wide variety of different effects. They do tend to have one of three characteristic pathological effects which characterize them as autoimmune diseases:[8]
- Damage to or destruction of tissues
- Altered organ growth
- Altered organ function
It has been estimated that autoimmune diseases are among the leading causes of death among women in the United States in all age groups up to 65 years.[9]
A substantial minority of the population suffers from these diseases, which are often chronic, debilitating, and life-threatening.[citation needed]
There are more than 80 illnesses caused by autoimmunity.[10]
Pathophysiology
The human immune system typically produces both T cells and B cells that are capable of being reactive with self-antigens, but these self-reactive cells are usually either killed prior to becoming active within the immune system, placed into a state of anergy (silently removed from their role within the immune system due to over-activation), or removed from their role within the immune system by regulatory cells. When any one of these mechanisms fail, it is possible to have a reservoir of self-reactive cells that become functional within the immune system. The mechanisms of preventing self-reactive T cells from being created takes place through negative selection process within the thymus as the T cell is developing into a mature immune cell.
Some infections, such as Campylobacter jejuni, have antigens that are similar (but not identical) to our own self-molecules. In this case, a normal immune response to C. jejuni can result in the production of antibodies that also react to a lesser degree with receptors on skeletal muscle (i.e., Myasthenia gravis). A major understanding of the underlying pathophysiology of autoimmune diseases has been the application of genome wide association scans that have identified a degree of genetic sharing among the autoimmune diseases.[11]
Autoimmunity, on the other hand, is the presence of self-reactive immune response (e.g., auto-antibodies, self-reactive T cells), with or without damage or pathology resulting from it.[12] This may be restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue in different places (e.g. Goodpasture's disease which may affect the basement membrane in both the lung and the kidney).
There are many theories as to how an autoimmune disease state arises. Some common ones are listed below.
Cryptic determinants/molecular sequestration
Although it is possible for a potential autoantigen to be spatially sequestered in an immune privileged site within the body (e.g. the eye), mechanisms exist to express even these antigens in a tolerogenic fashion to the immune system. However, it is impossible to induce tolerance (immune unresponsiveness) to all aspects of an autoantigen. This is because under normal physiologic conditions some regions of a self-antigen are not expressed at a sufficient level to induce tolerance. These poorly displayed areas of an antigen are called "cryptic determinants." The immune system maintains a high-affinity repertoire to the cryptic self because the presentation of these determinants was insufficient to induce strong tolerance.[13]
Molecular mimicry
The concept of molecular mimicry describes a situation in which a foreign antigen can initiate an immune response in which a T or B cell component cross-recognizes self. The cross reactive immune response is responsible for the autoimmune disease state.[14] Cross-reactive immune responses to self were first described for antibodies.
Altered glycan theory
According to this theory the effector function of the immune response is mediated by the glycans (polysaccharides) displayed by the cells and humoral components of the immune system. Individuals with autoimmunity have alterations in their glycosylation profile such that a proinflammatory immune response is favored. It is further hypothesized that individual autoimmune diseases will have unique glycan signatures.[15]
Hygiene hypothesis
According to the hygiene hypothesis, high levels of cleanliness expose children to fewer antigens than in the past, causing their immune systems to become overactive and more likely to misidentify own tissues as foreign, resulting in autoimmune conditions such as asthma.[16]
Epidemiology
The first estimate of US prevalence for autoimmune diseases as a group was published in 1997 by Jacobson, et al. They reported US prevalence to be around 9 million, applying prevalence estimates for 24 diseases to a US population of 279 million.[17] Jacobson's work was updated by Hayter & Cook in 2012.[18] This study used Witebsky's postulates, as revised by Rose & Bona,[19] to extend the list to 81 diseases and estimated overall cumulative US prevalence for the 81 autoimmune diseases at 5.0%, with 3.0% for males and 7.1% for females. The estimated community prevalence, which takes into account the observation that many people have more than one autoimmune disease, was 4.5% overall, with 2.7% for males and 6.4% for females.[18]
Research
In both autoimmune and inflammatory diseases, the condition arises through aberrant reactions of the human adaptive or innate immune systems. In autoimmunity, the patient's immune system is activated against the body's own proteins. In chronic inflammatory diseases, neutrophils and other leukocytes are constitutively recruited by cytokines and chemokines, leading to tissue damage.
Mitigation of inflammation by activation of anti-inflammatory genes and the suppression of inflammatory genes in immune cells is a promising therapeutic approach.[20][21][22] There is a body of evidence that once the production of autoantibodies has been initialized, autoantibodies have the capacity to maintain their own production.[23]
Stem cell transplantation is being studied and has shown promising results in certain cases.[24]
History
Traditionally it was believed that the immune system was unable to react against the body's own tissues, a concept described by the German immunologist Paul Ehrlich as "horror autotoxicus". In 1904 this theory was challenged by the discovery of a substance in the serum of patients with paroxysmal cold hemoglobinuria that reacted with red blood cells.[25]
References
- ^ a b c d e f g h i j k l m n o p q r "Autoimmune diseases fact sheet". OWH. 16 July 2012. Archived from the original on 5 October 2016. Retrieved 5 October 2016.
- ^ a b Katz, U; Shoenfeld, Y; Zandman-Goddard, G (2011). "Update on intravenous immunoglobulins (IVIg) mechanisms of action and off- label use in autoimmune diseases". Current pharmaceutical design. 17 (29): 3166–75. doi:10.2174/138161211798157540. PMID 21864262.
- ^ a b c d Borgelt, Laura Marie (2010). Women's Health Across the Lifespan: A Pharmacotherapeutic Approach. ASHP. p. 579. ISBN 9781585281947. Archived from the original on 2017-09-08.
- ^ Reinhard Hohlfeld, Klaus Dornmair, Edgar Mein, Hartmut Weker, The search for the target antigens of multiple sclerosis, part 1: autoreactive CD4+ T lymphocytes as pathogenic effectors and therapeutic targets. The Lancet, Neurology, Volume 15, Issue 2, February 2016, Pages 198-209, https://doi.org/10.1016/S1474-4422(15)00334-8
- ^ Paniker, Ananthanarayan And (169). Ananthanarayan and Paniker's Textbook of Microbiology. 2005: Orient Blackswan. ISBN 9788125028086. Archived from the original on 2017-09-08.
- ^ Witebsky E, Rose NR, Terplan K, Paine JR, Egan RW (1957). "Chronic thyroiditis and autoimmunization". J. Am. Med. Assoc. 164 (13): 1439–47. doi:10.1001/jama.1957.02980130015004. PMID 13448890.
- ^ Rose NR, Bona C (September 1993). "Defining criteria for autoimmune diseases (Witebsky's postulates revisited)". Immunol. Today. 14 (9): 426–30. doi:10.1016/0167-5699(93)90244-F. PMID 8216719.
- ^ "Autoimmune disorders: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Archived from the original on 2016-01-12. Retrieved 2016-01-21.
- ^ Walsh, SJ; Rau, LM (September 2000). "Autoimmune diseases: a leading cause of death among young and middle-aged women in the United States". American Journal of Public Health. 90 (9): 1463–6. doi:10.2105/ajph.90.9.1463. PMC 1447637 . PMID 10983209.
- ^ "MedlinePlus medical encyclopedia - autoimmune disorders". National Institutes of Health. 16 July 2014. Archived from the original on 5 January 2015. Retrieved 21 December 2014.
- ^ Cotsapas C, Hafler DA (2013). "Immune-mediated disease genetics: the shared basis of pathogenesis". Trends in Immunology. 34 (1): 22–6. doi:10.1016/j.it.2012.09.001. PMID 23031829.
- ^ Harrison's Principles of Internal Medicine: Volumes 1 and 2, 18th Edition (18 ed.). McGraw-Hill Professional. 2011-08-11. ISBN 9780071748896. Archived from the original on 2016-05-29.
- ^ Gammon G, Sercarz E (1989). "How some T cells escape tolerance induction". Nature. 342: 6246. doi:10.1038/342183a0. PMID 2478888.
- ^ Wucherpfennig KW, Strominger JL (1995). "Molecular mimicry in T cell-mediated autoimmunity: viral peptides activate human T cell clones specific for myelin basic protein". Cell. 80 (5): 695–705. doi:10.1016/0092-8674(95)90348-8. PMID 7534214.
- ^ Maverakis E, Kim K, Shimoda M, Gershwin M, Patel F, Wilken R, Raychaudhuri S, Ruhaak LR, Lebrilla CB (2015). "Glycans in the immune system and The Altered Glycan Theory of Autoimmunity". J Autoimmun. 57 (6): 1–13. doi:10.1016/j.jaut.2014.12.002. PMC 4340844 . PMID 25578468.
- ^ Rook, Graham A. W. (17 November 2011). "Hygiene Hypothesis and Autoimmune Diseases". Clinical Reviews in Allergy & Immunology. 42 (1): 5–15. doi:10.1007/s12016-011-8285-8. PMID 22090147.
- ^ Jacobson, DL; Gange, SJ; Rose, NR; Graham, NM (September 1997). "Epidemiology and estimated population burden of selected autoimmune diseases in the United States". Clinical immunology and immunopathology. 84 (3): 223–43. doi:10.1006/clin.1997.4412. PMID 9281381.
- ^ a b Hayter, SM; Cook, MC (August 2012). "Updated assessment of the prevalence, spectrum and case definition of autoimmune disease". Autoimmunity reviews. 11 (10): 754–65. doi:10.1016/j.autrev.2012.02.001. PMID 22387972.
- ^ Rose, NR; Bona, C (September 1993). "Defining criteria for autoimmune diseases (Witebsky's postulates revisited)". Immunology Today. 14 (9): 426–30. doi:10.1016/0167-5699(93)90244-F. PMID 8216719.
- ^ Mukundan L, Odegaard JI, Morel CR, Heredia JE, Mwangi JW, Ricardo-Gonzalez RR, Goh YP, Eagle AR, Dunn SE, et al. (Nov 2009). "PPAR-delta senses and orchestrates clearance of apoptotic cells to promote tolerance". Nat Med. 15 (11): 1266–72. doi:10.1038/nm.2048. PMC 2783696 . PMID 19838202.
- ^ Roszer T, Menéndez-Gutiérrez MP, Lefterova MI, Alameda D, Núñez V, Lazar MA, Fischer T, Ricote M (Jan 2011). "Autoimmune kidney disease and impaired engulfment of apoptotic cells in mice with macrophage peroxisome proliferator-activated receptor gamma or retinoid X receptor alpha deficiency". J Immunol. 186 (1): 621–31. doi:10.4049/jimmunol.1002230. PMID 21135166.
- ^ Singh RP, Waldron RT, Hahn BH (2012). "Genes, tolerance and systemic autoimmunity". Autoimmunity Reviews. 11 (9): 664–9. doi:10.1016/j.autrev.2011.11.017. PMC 3306516 . PMID 22155015.
- ^ Böhm I (2003). "Disruption of the cytoskeleton after apoptosis induction by autoantibodies". Autoimmunity. 36 (3): 183–9. PMID 12911286.
- ^ Swart, JF; Delemarre, EM; van Wijk, F; Boelens, JJ; Kuball, J; van Laar, JM; Wulffraat, NM (April 2017). "Haematopoietic stem cell transplantation for autoimmune diseases". Nature reviews. Rheumatology. 13 (4): 244–256. PMID 28228650.
- ^ Moticka, Edward J. (2013). Historical perspective on evidence-based immunology. Elsevier Science Publishing. p. 300. ISBN 9780123983817.
Further reading
- Vinay Kumar, Abul K. Abbas, Nelson Fausto, Jon Aster, Robbins and Cotran Pathologic Basis of Disease, Elsevier, 8th edition, 2010, 1464 pp., ISBN 978-1-4160-3121-5
- Handbook of Systemic Autoimmune Diseases, edited by Ronald Asherson, Elsevier, in 10 Volumes: http://www.elsevier.com/wps/find/bookdescription.cws_home/BS_HSAD/description#description
- Ronald Asherson, Andrea Doria, Paolo Pauletto, The Heart in Systemic Autoimmune Diseases, Volume 1, 2004, ISBN 978-0-444-51398-4, ISBN 0-444-51398-1
- Ronald Asherson, Andrea Doria, Paolo Pauletto, Pulmonary Involvement in Systemic Autoimmune Diseases, Volume 2, 2005, ISBN 978-0-444-51652-7, ISBN 0-444-51652-2
- Ronald Asherson, Doruk Erkan, Steven Levine, The Neurologic Involvement in Systemic Autoimmune Diseases, Volume 3, 2005, ISBN 978-0-444-51651-0, ISBN 0-444-51651-4
- Michael Lockshin, Ware Branch (eds), Reproductive and Hormonal Aspects of Systemic Autoimmune Diseases, Volume 4, 2006, ISBN 978-0-444-51801-9, ISBN 0-444-51801-0
- Piercarlo Sarzi-Puttini, Ronald Asherson, Andrea Doria, Annegret Kuhn, Giampietro Girolomoni (eds), The Skin in Systemic Autoimmune Diseases, Volume Volume 5, 2006, ISBN 978-0-444-52158-3, ISBN 0-444-52158-5
- Rolando Cimaz, Ronald Asherson, Thomas Lehman (eds), Pediatrics in Systemic Autoimmune Diseases, Volume 6, 2008, ISBN 978-0-444-52971-8, ISBN 0-444-52971-3
- Justin Mason, Ronald Asherson, Charles Pusey (eds), The Kidney in Systemic Autoimmune Diseases, Volume 7, 2008, ISBN 978-0-444-52972-5, ISBN 0-444-52972-1
- Ronald Asherson, Manel Ramos-Casals, Joan Rodes, Josep Font, Digestive Involvement in Systemic Autoimmune Diseases, Volume 8, 2008, ISBN 978-0-444-53168-1, ISBN 0-444-53168-8
- Ronald Asherson, Sara Walker, Luis Jara, Endocrine Manifestations of Systemic Autoimmune Diseases, Volume 9, 2008, ISBN 978-0-444-53172-8, ISBN 0-444-53172-6
- R. Cervera, Ronald Asherson, Munther Khamashta, Joan Carles Reverter (eds), Antiphospholipid Syndrome in Systemic Autoimmune Diseases, Volume 10, 2009, ISBN 978-0-444-53169-8, ISBN 0-444-53169-6
External links
Classification |
V · T · D
|
---|---|
External resources |
|
- Autoimmune disorders at Curlie (based on DMOZ)
Hypersensitivity and autoimmune diseases (279.5–6)
|
|||||||||
---|---|---|---|---|---|---|---|---|---|
Type I/allergy/atopy (IgE) |
|
||||||||
Type II/ADCC
|
|
||||||||
Type III (Immune complex) |
|
||||||||
Type IV/cell-mediated (T cells) |
|
||||||||
Unknown/ multiple |
|
- Biology portal
- Medicine portal
Authority control |
|
---|
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2018/04/25 20:05:04」(JST)
wiki en
[Wiki en表示]Autoimmune diseases | |
---|---|
Young woman with the typical "butterfly rash" found in lupus | |
Specialty | Rheumatology, immunology, gastroenterology, other |
Symptoms | Depends on the condition. Commonly low grade fever, feeling tired[1] |
Usual onset | Adulthood[1] |
Types | Alopecia areata, celiac disease, diabetes mellitus type 1, Graves' disease, inflammatory bowel disease, multiple sclerosis, psoriasis, rheumatoid arthritis, systemic lupus erythematosus, others[1] |
Medication | Nonsteroidal anti-inflammatory drugs, immunosuppressants, intravenous immunoglobulin[1][2] |
Frequency | 24 million / 7% (USA)[1][3] |
An autoimmune disease is a condition arising from an abnormal immune response to a normal body part.[1] There are at least 80 types of autoimmune diseases.[1] Nearly any body part can be involved.[3] Common symptoms include low grade fever and feeling tired.[1] Often symptoms come and go.[1]
The cause is generally unknown.[3] Some autoimmune diseases such as lupus run in families, and certain cases may be triggered by infections or other environmental factors.[1] Some common diseases that are generally considered autoimmune include celiac disease, diabetes mellitus type 1, Graves' disease, inflammatory bowel disease, multiple sclerosis, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus.[1][4] The diagnosis can be difficult to determine.[1]
Treatment depends on the type and severity of the condition.[1] Nonsteroidal anti-inflammatory drugs (NSAIDs) and immunosuppressants are often used.[1] Intravenous immunoglobulin may also occasionally be used.[2] While treatment usually improves symptoms they do not typically cure the disease.[1]
About 24 million (7%) people in the United States are affected by an autoimmune disease.[1][3] Women are more commonly affected than men.[1] Often they start during adulthood.[1] The first autoimmune diseases were described in the early 1900s.[5]
Contents
- 1 Definition
- 2 Signs and symptoms
- 3 Pathophysiology
- 3.1 Cryptic determinants/molecular sequestration
- 3.2 Molecular mimicry
- 3.3 Altered glycan theory
- 3.4 Hygiene hypothesis
- 4 Epidemiology
- 5 Research
- 6 History
- 7 References
- 8 Further reading
- 9 External links
Definition
For a disease to be regarded as an autoimmune disease it needs to answer to Witebsky's postulates (first formulated by Ernest Witebsky and colleagues in 1957 and modified in 1994):[6][7]
- Direct evidence from transfer of disease-causing antibody or disease-causing T lymphocyte white blood cells
- Indirect evidence based on reproduction of the autoimmune disease in experimental animals
- Circumstantial evidence from clinical clues
- Genetic evidence suggesting "clustering" with other autoimmune diseases
Signs and symptoms
Autoimmune diseases have a wide variety of different effects. They do tend to have one of three characteristic pathological effects which characterize them as autoimmune diseases:[8]
- Damage to or destruction of tissues
- Altered organ growth
- Altered organ function
It has been estimated that autoimmune diseases are among the leading causes of death among women in the United States in all age groups up to 65 years.[9]
A substantial minority of the population suffers from these diseases, which are often chronic, debilitating, and life-threatening.[citation needed]
There are more than 80 illnesses caused by autoimmunity.[10]
Pathophysiology
The human immune system typically produces both T cells and B cells that are capable of being reactive with self-antigens, but these self-reactive cells are usually either killed prior to becoming active within the immune system, placed into a state of anergy (silently removed from their role within the immune system due to over-activation), or removed from their role within the immune system by regulatory cells. When any one of these mechanisms fail, it is possible to have a reservoir of self-reactive cells that become functional within the immune system. The mechanisms of preventing self-reactive T cells from being created takes place through negative selection process within the thymus as the T cell is developing into a mature immune cell.
Some infections, such as Campylobacter jejuni, have antigens that are similar (but not identical) to our own self-molecules. In this case, a normal immune response to C. jejuni can result in the production of antibodies that also react to a lesser degree with receptors on skeletal muscle (i.e., myasthenia gravis). A major understanding of the underlying pathophysiology of autoimmune diseases has been the application of genome wide association scans that have identified a degree of genetic sharing among the autoimmune diseases.[11]
Autoimmunity, on the other hand, is the presence of self-reactive immune response (e.g., auto-antibodies, self-reactive T cells), with or without damage or pathology resulting from it.[12] This may be restricted to certain organs (e.g. in autoimmune thyroiditis) or involve a particular tissue in different places (e.g. Goodpasture's disease which may affect the basement membrane in both the lung and the kidney).
There are many theories as to how an autoimmune disease state arises. Some common ones are listed below.
Cryptic determinants/molecular sequestration
Although it is possible for a potential autoantigen to be spatially sequestered in an immune privileged site within the body (e.g. the eye), mechanisms exist to express even these antigens in a tolerogenic fashion to the immune system. However, it is impossible to induce tolerance (immune unresponsiveness) to all aspects of an autoantigen. This is because under normal physiologic conditions some regions of a self-antigen are not expressed at a sufficient level to induce tolerance. These poorly displayed areas of an antigen are called "cryptic determinants." The immune system maintains a high-affinity repertoire to the cryptic self because the presentation of these determinants was insufficient to induce strong tolerance.[13]
Molecular mimicry
The concept of molecular mimicry describes a situation in which a foreign antigen can initiate an immune response in which a T or B cell component cross-recognizes self. The cross reactive immune response is responsible for the autoimmune disease state.[14] Cross-reactive immune responses to self were first described for antibodies.
Altered glycan theory
According to this theory the effector function of the immune response is mediated by the glycans (polysaccharides) displayed by the cells and humoral components of the immune system. Individuals with autoimmunity have alterations in their glycosylation profile such that a proinflammatory immune response is favored. It is further hypothesized that individual autoimmune diseases will have unique glycan signatures.[15]
Hygiene hypothesis
According to the hygiene hypothesis, high levels of cleanliness expose children to fewer antigens than in the past, causing their immune systems to become overactive and more likely to misidentify own tissues as foreign, resulting in autoimmune conditions such as asthma.[16]
Epidemiology
The first estimate of US prevalence for autoimmune diseases as a group was published in 1997 by Jacobson, et al. They reported US prevalence to be around 9 million, applying prevalence estimates for 24 diseases to a US population of 279 million.[17] Jacobson's work was updated by Hayter & Cook in 2012.[18] This study used Witebsky's postulates, as revised by Rose & Bona,[19] to extend the list to 81 diseases and estimated overall cumulative US prevalence for the 81 autoimmune diseases at 5.0%, with 3.0% for males and 7.1% for females. The estimated community prevalence, which takes into account the observation that many people have more than one autoimmune disease, was 4.5% overall, with 2.7% for males and 6.4% for females.[18]
Research
In both autoimmune and inflammatory diseases, the condition arises through aberrant reactions of the human adaptive or innate immune systems. In autoimmunity, the patient's immune system is activated against the body's own proteins. In chronic inflammatory diseases, neutrophils and other leukocytes are constitutively recruited by cytokines and chemokines, leading to tissue damage.
Mitigation of inflammation by activation of anti-inflammatory genes and the suppression of inflammatory genes in immune cells is a promising therapeutic approach.[20][21][22] There is a body of evidence that once the production of autoantibodies has been initialized, autoantibodies have the capacity to maintain their own production.[23]
Stem cell transplantation is being studied and has shown promising results in certain cases.[24]
History
Traditionally it was believed that the immune system was unable to react against the body's own tissues, a concept described by the German immunologist Paul Ehrlich as "horror autotoxicus". In 1904 this theory was challenged by the discovery of a substance in the serum of patients with paroxysmal cold hemoglobinuria that reacted with red blood cells.[25]
References
- ^ a b c d e f g h i j k l m n o p q r "Autoimmune diseases fact sheet". OWH. 16 July 2012. Archived from the original on 5 October 2016. Retrieved 5 October 2016.
- ^ a b Katz, U; Shoenfeld, Y; Zandman-Goddard, G (2011). "Update on intravenous immunoglobulins (IVIg) mechanisms of action and off- label use in autoimmune diseases". Current pharmaceutical design. 17 (29): 3166–75. doi:10.2174/138161211798157540. PMID 21864262.
- ^ a b c d Borgelt, Laura Marie (2010). Women's Health Across the Lifespan: A Pharmacotherapeutic Approach. ASHP. p. 579. ISBN 9781585281947. Archived from the original on 2017-09-08.
- ^ Reinhard Hohlfeld, Klaus Dornmair, Edgar Mein, Hartmut Weker, The search for the target antigens of multiple sclerosis, part 1: autoreactive CD4+ T lymphocytes as pathogenic effectors and therapeutic targets. The Lancet, Neurology, Volume 15, Issue 2, February 2016, Pages 198-209, https://doi.org/10.1016/S1474-4422(15)00334-8
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Further reading
- Vinay Kumar, Abul K. Abbas, Nelson Fausto, Jon Aster, Robbins and Cotran Pathologic Basis of Disease, Elsevier, 8th edition, 2010, 1464 pp., ISBN 978-1-4160-3121-5
- Handbook of Systemic Autoimmune Diseases, edited by Ronald Asherson, Elsevier, in 10 Volumes: http://www.elsevier.com/wps/find/bookdescription.cws_home/BS_HSAD/description#description
External links
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UpToDate Contents
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- 1. 未分化型の全身性リウマチ性(結合組織)疾患およびオーバーラップ症候群 undifferentiated systemic rheumatic connective tissue diseases and overlap syndromes
- 2. 自己免疫の概要 overview of autoimmunity
- 3. 混合性結合組織病の定義および診断 definition and diagnosis of mixed connective tissue disease
- 4. 抗核抗体の測定および臨床的意義 measurement and clinical significance of antinuclear antibodies
- 5. 混合性結合組織病の臨床症状 clinical manifestations of mixed connective tissue disease
英文文献
- Lack of HLA predominance and HLA shared epitopes in biliary Atresia.
- Mack CL, Anderson KM, Aubrey MT, Rosenthal P, Sokol RJ, Freed BM.SourceDepartments of Medicine and Immunology, Division of Allergy and Clinical Immunology, University of Colorado School of Medicine, 80045 Aurora, CO USA ; Department of Pediatrics, Division of Pediatric Gastroenterology, Digestive Health Institute, Children's Hospital Colorado, Hepatology and Nutrition, 13123 East 16th Ave. B290, 80045 Aurora, CO USA.
- SpringerPlus.Springerplus.2013 Dec;2(1):42. Epub 2013 Feb 8.
- Biliary atresia (BA) is characterized by progressive inflammation and fibrosis of bile ducts. A theory of pathogenesis entails autoimmune-mediated injury targeting bile duct epithelia. One of the strongest genetic associations with autoimmunity is with HLA genes. In addition, apparently dissimilar H
- PMID 23505615
- Warthin's tumor associated with IgG4-related disease.
- Aga M, Kondo S, Yamada K, Sawada-Kitamura S, Yagi-Nakanishi S, Endo K, Wakisaka N, Murono S, Kawano M, Yoshizaki T.SourceDivision of Otolaryngology, Graduate School of Medicine, Kanazawa University, Kanazawa, Japan.
- Auris, nasus, larynx.Auris Nasus Larynx.2013 Oct;40(5):514-7. doi: 10.1016/j.anl.2012.11.005. Epub 2012 Dec 13.
- Immunoglobulin G4-related disease (IgG4-RD) is an inflammatory condition associated with elevated serum IgG4 levels and tissue infiltration by IgG4-expressing plasma cells. Several inflammatory conditions associated with IgG4-RD have been reported. Warthin's tumor is a benign parotid gland tumor con
- PMID 23246115
- α-Lipoic acid enhances endogenous peroxisome-proliferator-activated receptor-γ to ameliorate experimental autoimmune encephalomyelitis in mice.
- Wang KC, Tsai CP, Lee CL, Chen SY, Lin GJ, Yen MH, Sytwu HK, Chen SJ.Source¶School of Medicine, Fu-Jen Catholic University, Taipei, Taiwan.
- Clinical science (London, England : 1979).Clin Sci (Lond).2013 Oct 1;125(7):329-40. doi: 10.1042/CS20120560.
- ALA (α-lipoic acid) is a natural, endogenous antioxidant that acts as a PPAR-γ (peroxisome-proliferator-activated receptor-γ) agonist to counteract oxidative stress. Thus far, the antioxidative and immunomodulatory effects of ALA on EAE (experimental autoimmune encephalomyelitis) are not well und
- PMID 23550596
和文文献
- 後天性血友病A:第VIII因子インヒビター
- 森 直樹
- 東京女子医科大学雑誌 83(E2), E508-E511, 2013-03-31
- 凝固第VIII因子に対する自己抗体に伴う出血傾向は後天性血友病Aとして知られている。発生頻度は0.5〜1人/100万人と稀で、20〜30歳と60〜80歳に多い。基礎疾患としては自己免疫疾患、悪性腫瘍があり、妊娠や薬剤使用に伴うこともある。高齢者では基礎疾患を伴わないものが多い。,臨床症状は皮下出血、筋肉内出血、消化管出血、中枢神経系出血などであるが、先天性血友病と比べて関節内出血は多くない。重症の …
- NAID 110009575060
- 新たな疾患概念,IgG4関連疾患の危険選択
- 渡邊 岳博
- 日本保険医学会誌 111(1), 48-71, 2013-03-29
- IgG4関連疾患は日本より近年発信された新しい疾患概念である。従来自己免疫性膵炎や後腹膜線維症等と別々の疾患と考えられていた病態がIgG4関連疾患という概念に統一できることが明らかになった。本疾患の包括診断基準が2012年に発表され,今後広く普及していくものと推測される。唾液腺,膵臓,腎臓では臓器毎の診断基準と併用も可能で診断が容易となった。日々の査定においても本疾患あるいは本疾患と思われる診断書 …
- NAID 110009603875
- Three Groups in the 28 Joints for Rheumatoid Arthritis Synovitis - Analysis Using More than 17,000 Assessments in the KURAMA Database.
- Terao Chikashi,Hashimoto Motomu,Yamamoto Keiichi,Murakami Kosaku,Ohmura Koichiro,Nakashima Ran,Yamakawa Noriyuki,Yoshifuji Hajime,Yukawa Naoichiro,Kawabata Daisuke,Usui Takashi,Yoshitomi Hiroyuki,Furu Moritoshi,Yamada Ryo,Matsuda Fumihiko,Ito Hiromu,Fujii Takao,Mimori Tsuneyo
- PloS one 8(3), 2013-03-12
- … Rheumatoid arthritis (RA) is a joint-destructive autoimmune disease. …
- NAID 120005244457
関連画像
■★リンクテーブル★
「自己免疫疾患」
- 英
- autoimmune disease
- 関
- [[]]
- 全身性自己免疫疾患
- 臓器特異的自己免疫疾患
「nervous system autoimmune disease」
「autoimmune diseases of the nervous system」
「CNS demyelinating autoimmune disease」
「experimental nervous system autoimmune disease」
「disease」
- n.
- 疾患:illnessより厳密な概念。「ある臓器に明確な障害が確認され、それによって症状が出ているとはっきり説明できる場合」 (PSY.9)
- 特定の原因、病態生理、症状、経過、予後、病理組織所見が全てそろった場合 (PSY.9)
- something that is very wrong with people's attitudes, way of life or with society.
- 注意
WordNet [license wordnet]
「an impairment of health or a condition of abnormal functioning」PrepTutorEJDIC [license prepejdic]
「(体の)『病気』,疾患 / (精神・道徳などの)病気,病弊」PrepTutorEJDIC [license prepejdic]
「女性の話術芸人 =diseur」
「diseased」
WordNet [license wordnet]
「caused by or altered by or manifesting disease or pathology; "diseased tonsils"; "a morbid growth"; "pathologic tissue"; "pathological bodily processes"」PrepTutorEJDIC [license prepejdic]
「病気にかかった / 病的な,不健全な(morbid)」
「autoimmune」
WordNet [license wordnet]
「of or relating to the immune response of the body against substance normally present in the body」