体液性免疫不全、体液性免疫不全症

WordNet

put into a good mood (同)humour
the trait of appreciating (and being able to express) the humorous; "she didnt appreciate my humor"; "you cant survive in the army without a sense of humor" (同)humour, sense of humor, sense of humour
(Middle Ages) one of the four fluids in the body whose balance was believed to determine your emotional and physical state; "the humors are blood and phlegm and yellow and black bile" (同)humour
the quality of being funny; "I fail to see the humor in it" (同)humour
(medicine) the condition in which an organism can resist disease (同)resistance
the quality of being unaffected by something; "immunity to criticism"

PrepTutorEJDIC

《所有・所属》…『の』,…のものである,…に属する・《材料・要素》…『でできた』,から成る・《部分》…『の』[『中の』] ・《数量・単位・種類を表す名詞に付いて》…の・《原因・動機》…『で』,のために(because of) ・《主格関係》…『の』,による,によって・《目的格関係》…『を』,の・《同格関係》…『という』・《関係・関連》…『についての』[『の』],の点で・《抽象名詞などと共に》…の[性質をもつ] ・《『It is』+『形』+『of』+『名』+『to』 doの形で,ofの後の名詞を意味上の主語として》・《分離》…『から』・《起原・出所》…『から』[『の』](out of) ・《『名』+『of』+『a』(『an』)+『名』の形で》…のような・《『名』+『of』+『mine』(『yours, his』など独立所有格)の形で》…の…・《時》(1)《副詞句を作って》…に《形容詞句を作って》…の・《時刻》《米》…前(to,《米》before)
〈U〉〈C〉(…の)(量・額などの)不足,欠乏《+『of』(『in』)+『名』》 / 〈C〉不足分,不足量,不足額 / 〈C〉(精神・肉体などの)欠陥
〈U〉(病気に対する)免疫《+『from』(『to, against』)+『名』》 / (義務・税などの)免除《+『from』(『to, against』)+『名』》
OLD French古[代]フランス語

UpToDate Contents

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1. 原発性の体液性免疫不全：概要 primary humoral immune deficiencies an overview
2. 体液性免疫応答 the humoral immune response
3. 高IgM症候群 hyperimmunoglobulin m syndrome
4. 同種造血細胞移植後の免疫再構築のための戦略 strategies for immune reconstitution following allogeneic hematopoietic cell transplantation
5. IgG サブクラス欠乏症 igg subclass deficiency

English Journal

Brain abscess caused by Nocardia cyriacigeorgica in two patients with multiple myeloma: novel agents, new spectrum of infections.

Pamukçuoğlu M, Emmez H, Tunçcan OG, Oner AY, Cırak MY, Senol E, Sucak GT.AbstractObjective and importance Introduction of high-dose chemotherapy and the novel agents including bortezomib, Lenalidomide, and Thalidomide has provided a significant progress in the treatment of multiple myeloma (MM) with an increase in median overall survival up to 6-8 years. However, the advances in myeloma treatment comes at a price with new spectrum of treatment-related infectious complications which should be taken into consideration while treating these patients. Clinical presentation We report here two patients with Ig G λ MM presenting with intracerebral mass lesions in the abscence of constitutional symptoms that would suggest an infectious etiology. Both patients had severe hypogammaglobulinemia and lymphopenia, which was attributed to treatment regimens including bortezomib. Intervention The surgical intervention-revealed abscess in both cases caused by Nocardia cyriacigeorgica, a relatively new pathogen which rarely causes infections in humans and also an unexpected pathogen in myeloma patients. Conclusion Although every aspect of immune system is known to be affected in MM, humoral immune deficiency is the hallmark of the inherent immune defect in this disease. Introduction of the novel agents, bortezomib in particular seems to have changed the characteristics of the immune dysfunction and the spectrum of the opportunistic infections by causing qualitative and quantitative changes in cellular immunity. The new spectrum of infectious agents might not be limited to hepatitis B and herpes zoster. Monitoring lymphopenia and administration of prophylactic antimicrobial agents accordingly could be considered in patients treated with bortezomib.
Hematology (Amsterdam, Netherlands).Hematology.2014 Apr;19(3):158-62. doi: 10.1179/1607845413Y.0000000108. Epub 2013 Nov 25.
Objective and importance Introduction of high-dose chemotherapy and the novel agents including bortezomib, Lenalidomide, and Thalidomide has provided a significant progress in the treatment of multiple myeloma (MM) with an increase in median overall survival up to 6-8 years. However, the advances in
PMID 23906027

Successful Haploidentical Hematopoietic Stem Cell Transplantation in a Patient with SCID due to CD3ε Deficiency: Need for IgG-Substitution 6 Years Later.

Fuehrer M1, Pannicke U1, Schuetz C2, Jacobsen EM2, Schulz A2, Friedrich W2, Schwarz K1, Hönig M2.Author information 1Institute of Transfusion Medicine, University Ulm, Germany.2Department of Pediatrics and Adolescent Medicine, University Medical Center Ulm, Germany.AbstractThe CD3 co-receptor complex is essential for signal transduction after specific binding of the T-cell receptor (TCR). CD3E encodes the CD3ε chain, one of the protein components (γ-, δ-, ε- and ζ-chain) of the CD3 co-receptor. As previously reported in one family CD3ε deficiency causes SCID.We report on a patient with SCID due to CD3ε deficiency treated by HLA-haploidentical stem cell transplantation (SCT) (donor: mother) 15 years ago which resulted in development of normal T- and B-cell immunity. Despite conditioning donor cell engraftment was confined to T cells, while all other blood cell lineages remained of patient origin (split chimerism). In spite of normal functions, T-cell numbers never reached normal levels and naïve CD45+RA+ T-cells remained low. At 6 years after SCT the patient developed signs of humoral immunodeficiency, requiring regular substitution of IgG.In a retrospective genetic work up 11 years after SCT, a homozygous splice site mutation in CD3E was identified resulting in the loss of CD3ε protein. The loss of B-cell function as observed in the patient was reflected by a lack of switched memory B cells. To rule out a primary role of CD3ε in B-cell function we studied expression of CD3E in B-cells which was found not to be expressed.The clinical presentation of a secondary loss of specific humoral immunity in this constellation of split chimerism after allogeneic haploidentical SCT is unusual and unexpected in a patient with a primary T-cell defect. A most likely explanation is the gradual loss of T-helper-cell function.
Klinische Padiatrie.Klin Padiatr.2014 Feb 10. [Epub ahead of print]
The CD3 co-receptor complex is essential for signal transduction after specific binding of the T-cell receptor (TCR). CD3E encodes the CD3ε chain, one of the protein components (γ-, δ-, ε- and ζ-chain) of the CD3 co-receptor. As previously reported in one family CD3ε deficiency causes SCID.We
PMID 24515816

Kupffer cell-derived IL-10 plays a key role in maintaining humoral immune tolerance in hepatitis B virus-persistent mice.

Xu L1, Yin W, Sun R, Wei H, Tian Z.Author information 1Department of Immunology, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, China.AbstractThe liver is considered as a unique lymphoid organ favoring the induction of immune tolerance, rather than immunity. Biologists and clinicians alike have a long-standing interest in how the liver induces systemic immune tolerance, but the mechanism has not yet been well elucidated. Here, we employed hepatitis B virus (HBV)-carrier mice generated by hydrodynamically injecting phosphor-adeno-associated virus/HBV1.2 plasmid as a model for adult chronic HBV infection, which we found were unable to respond to hepatitis B surface antigen vaccination. Humoral tolerance induced in HBV-carrier mice could be transferred into Rag1(-/-) mice, because anti-HBV immunity in immunologically reconstituted Rag1(-/-) mice was inhibited by adoptive transfer of splenocytes from HBV-carrier mice. Humoral tolerance needed at least 7 days for induction and persisted to 3 months after a single HBV plasmid injection. Kupffer cell (KC) depletion or interleukin (IL-10) deficiency broke this humoral tolerance, and exogenous injection of IL-10 could effectively induce this tolerance.
Hepatology (Baltimore, Md.).Hepatology.2014 Feb;59(2):443-52. doi: 10.1002/hep.26668. Epub 2013 Dec 24.
The liver is considered as a unique lymphoid organ favoring the induction of immune tolerance, rather than immunity. Biologists and clinicians alike have a long-standing interest in how the liver induces systemic immune tolerance, but the mechanism has not yet been well elucidated. Here, we employed
PMID 23929689

Japanese Journal

Relapsing Campylobacter Coli Bacteremia with Reactive Arthritis in a Patient with X-linked Agammaglobulinemia

Internal Medicine 46(9), 605-609, 2007
NAID 130000078723

Morphological Quantitative Changes in the Number of Lymphocytes, Macrophages and Plasma Cells in the Uterus and Lymph Nodes of Rats Exposed to the Systemic Administration of BCG