insulitis

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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 13:47:10」(JST)

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Insulitis is an inflammation of the islets of Langerhans of the pancreas.^[1] Pancreatic β-cells become infiltrated by mononuclear cells, leading to inflammation. This lymphocyte infiltration can result in destruction of the insulin producing beta cells of the islets,^[2] and clinical diabetes. Insulitis can be studied in the NOD mouse model of type-1 diabetes.

References

^ "insulitis" at Dorland's Medical Dictionary
^ In't Veld P, Lievens D, De Grijse J, et al (September 2007). "Screening for insulitis in adult autoantibody-positive organ donors". Diabetes 56 (9): 2400–4. doi:10.2337/db07-0416. PMID 17563060.

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1. 1型糖尿病の病因 pathogenesis of type 1 diabetes mellitus
2. 糖尿病を合併した腎臓・膵臓移植での患者選択とそれに関連する免疫学的問題 patient selection for and immunologic issues relating to kidney pancreas transplantation in diabetes mellitus
3. 1型糖尿病の予測 prediction of type 1 diabetes mellitus
4. 1型糖尿病の予防 prevention of type 1 diabetes mellitus
5. バセドウ病（グレーブス病）の発症機序 pathogenesis of graves disease

English Journal

A maternal gluten-free diet reduces inflammation and diabetes incidence in the offspring of NOD mice.

Hansen CH1, Krych L, Buschard K, Metzdorff SB, Nellemann C, Hansen LH, Nielsen DS, Frøkiær H, Skov S, Hansen AK.Author information 1Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, 1871 Frederiksberg C, Denmark.AbstractEarly life interventions in the intestinal environment have previously been shown to influence diabetes incidence. We therefore hypothesized that a gluten-free (GF) diet, known to decrease type 1 diabetes incidence, only during pregnancy and lactation period would protect against development of diabetes. Pregnant non-obese diabetic (NOD) mice were fed GF or standard diet, until all pups were weaned to standard diet. The early life GF environment dramatically decreased diabetes incidence and insulitis. Gut microbiota analysis by 16S rRNA gene sequencing revealed a pronounced difference between both mothers and their offspring, characterized by increased Akkermansia, Proteobacteria, and TM7 in the GF diet group. In addition, pancreatic FoxP3 regulatory T cells were increased in GF fed offspring; as were M2 macrophage gene markers and tight junction-related genes in the gut, while intestinal gene expression of proinflammatory cytokines was reduced. Increased proportion of T cells in the pancreas expressing the mucosal integrin α4β7 suggests that the mechanism involve increased trafficking of gut-primed immune cells to the pancreas. In conclusion, GF diet during fetal and early postnatal life reduces development of diabetes. The mechanism may involve a changed gut microbiota and shifts to a less proinflammatory immunological milieu in the gut and pancreas.
Diabetes.Diabetes.2014 Apr 2. [Epub ahead of print]
Early life interventions in the intestinal environment have previously been shown to influence diabetes incidence. We therefore hypothesized that a gluten-free (GF) diet, known to decrease type 1 diabetes incidence, only during pregnancy and lactation period would protect against development of diab
PMID 24696449

IRAK-M deficiency promotes the development of T1DM in NOD mice.

Tan Q1, Majewska-Szczepanik M, Zhang X, Szczepanik M, Zhou Z, Wong FS, Wen L.Author information 1Institution of Metabolism and Endocrinology, the Second Xiangya Hospital, Central South University, Changsha, China.AbstractType 1 diabetes mellitus (T1DM) is an organ specific autoimmune disease characterized by progressive destruction of insulin-secreting pancreatic beta cells. Both T cell mediated adaptive responses, as well as innate immune processes are involved in pathogenesis. Interleukin-1 receptor associated kinase M (IRAK-M) can effectively inhibit the MyD88 downstream signals in TLR pathways, while lack of IRAK-M is known to be associated with autoimmunity. Our study showed that IRAK-M deficient (IRAK-M-/-) non obese diabetic (NOD) mice displayed early onset and rapid progression of T1DM with impaired glucose tolerance, more severe insulitis and increased serum anti-insulin auto-antibodies. Mechanistic studies showed that enhanced activation and antigen presenting function of IRAK-M deficient antigen presenting cells (APCs) from IRAK-M-/- mice were responsible for rapid progression of disease. Moreover, IRAK-M-/- dendritic cells (DCs) induced enhanced activation of diabetogenic T cells in vitro and rapid onset of T1DM in vivo in immunodeficient NOD mice when co-transferred with diabetogenic T cells. This study illustrates how modulation of innate immune pathways through IRAK-M influences the development of autoimmune diabetes.
Diabetes.Diabetes.2014 Apr 2. [Epub ahead of print]
Type 1 diabetes mellitus (T1DM) is an organ specific autoimmune disease characterized by progressive destruction of insulin-secreting pancreatic beta cells. Both T cell mediated adaptive responses, as well as innate immune processes are involved in pathogenesis. Interleukin-1 receptor associated kin
PMID 24696448

Positivity for islet cell autoantibodies in patients with monogenic diabetes is associated with later diabetes onset and higher HbA1c level.

Urbanová J1, Rypáčková B, Procházková Z, Kučera P, Cerná M, Anděl M, Heneberg P.Author information 1Charles University in Prague, Third Faculty of Medicine, Prague, Czech Republic.AbstractAIMS: Islet cell autoantibodies are associated with autoimmune insulitis and belong to the diagnostic criteria of Type 1 diabetes mellitus. However, growing evidence suggests that autoantibodies are present in other types of diabetes. Here, we focus on the autoantibody incidence in Czech patients with maturity-onset diabetes of the young and analyse their functional relevance in terms of diabetes onset and control.
Diabetic medicine : a journal of the British Diabetic Association.Diabet Med.2014 Apr;31(4):466-71. doi: 10.1111/dme.12314. Epub 2013 Oct 16.
AIMS: Islet cell autoantibodies are associated with autoimmune insulitis and belong to the diagnostic criteria of Type 1 diabetes mellitus. However, growing evidence suggests that autoantibodies are present in other types of diabetes. Here, we focus on the autoantibody incidence in Czech patients w
PMID 24102923