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Contribution of T cells to the development of autoimmune diabetes in the NOD mouse model
Author(s) -
Toyoda Hiroo,
Formby Bent
Publication year - 1998
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/(sici)1521-1878(199809)20:9<750::aid-bies8>3.0.co;2-k
Subject(s) - nod , autoimmune diabetes , nod mice , diabetes mellitus , immunology , autoimmunity , biology , computational biology , medicine , immune system , endocrinology
The nonobese diabetic (NOD) mouse spontaneously develops an autoimmune diabetes that shares many immunogenetic features with human insulin‐dependent diabetes mellitus (IDDM), type 1 diabetes. The mononuclear cell infiltrates in the islet, which results in the development of insulitis (a prerequisite step for the development of diabetes) are primarily composed of T cells. It is now well accepted that these T cells play important roles in initiating and propagating an autoimmune process, which in turn destroys insulin‐producing islet β cells in the pancreas. T cells are subdivided into CD4 + helper T cells and CD8 + cytotoxic T cells. CD4 + T cells are further subdivided into Th1 and Th2 cells based on profiles of cytokine production, and these two T‐cell populations counterregulate each other. Because many autoimmune diseases are Th1 T‐cell mediated, current studies have focused on manipulating the Th1/Th2 imbalance to suppress the autoimmune process in the NOD model. Furthermore, the incidence of disease is much higher in females than that in males, suggesting an involvement of sex‐steroid hormones in the development of diabetes. Understanding insights of the mechanism of immune‐mediated islet cell destruction and the interaction between the immune and the neuroendocrine system may, therefore, provide new therapeutic means of preventing this chronic debilitating disease. BioEssays 20 :750–757, 1998. © 1998 John Wiley & Sons, Inc.