Autoimmunity Triggers in the NOD Mouse A Role for Natural Auto-antibody Reactivities in Type 1 Diabetes

被引：10

作者：

Corte-Real, Joana ^{[1
]}

Duarte, Nadia ^{[1
]}

Tavares, Luis ^{[2
]}

Penha-Goncalves, Carlos ^{[1
]}

机构：

[1] Inst Gulbenkian Ciencias, P-2781901 Oeiras, Portugal

[2] Fac Med Vet, CIISA, Lisbon, Portugal

来源：

CONTEMPORARY CHALLENGES IN AUTOIMMUNITY | 2009年 / 1173卷

关键词：

type; 1; diabetes; NOD; natural auto-antibodies; GLUTAMIC-ACID DECARBOXYLASE; PANCREATIC BETA-CELLS; B-CELLS; MICE; INSULIN; EXPRESSION; RECEPTORS; DISEASE; EPITOPE; IGM;

D O I：

10.1111/j.1749-6632.2009.04661.x

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The nonobese diabetic mouse (NOD) is widely used as a model to study human type I diabetes (T1D). In the NOD mouse T1D is a T cell-mediated autoimmune disease of complex etiology in which B cells play an essential role. One of the major unresolved issues in T1D is the genetic and/or environmental factors that trigger the autoimmune reaction. In the NOD mouse, as in humans, auto-antibodies to pancreatic islets are present at early ages and are highly correlated to diabetes progression, but their etiological role has long been disputed. NOD auto-antibodies have the characteristics of a natural repertoire, and B1 cells, the main natural antibody producers, exhibit functional differences in this strain that could have consequences for disease determination. Using a genetic approach, we propose to test if the NOD natural auto-antibody repertoire includes innate reactivities that participate in diabetes pathogenesis by promoting insulitis initiation.

引用

页码：442 / 448

页数：7

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