Premium
Autoimmunity Triggers in the NOD Mouse
Author(s) -
CôrteReal Joana,
Duarte Nádia,
Tavares Luís,
PenhaGonçalves Carlos
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.04661.x
Subject(s) - nod , insulitis , autoimmunity , immunology , nod mice , antibody , pathogenesis , biology , autoimmune disease , type 1 diabetes , innate immune system , diabetes mellitus , immune system , endocrinology
The nonobese diabetic mouse (NOD) is widely used as a model to study human type 1 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.