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The development of insulin-dependent diabetes mellitus in non-obese diabetic mice: the role of CD4+ and CD8+ T cells.

Introduction The non-obese diabetic (NOD) mouse is a spontaneous animal model of the human autoimmune disease, insulin-dependent diabetes mellitus (IDDM) [ 11. In this mouse model, mononuclear cell infiltration in the pancreas is evident in both sexes from 5 to 6 weeks of age. Disease development resulting from a progressive intra-islet infiltration and B-cell destruction occurs in many colonies, predominantly in female mice, from 30 weeks of age. The development of IDDM in the NOD mouse is dependent on T cells and the disease can be passively transferred by a combination of CD4 + and CD8 + splenic T cells from a diabetic donor but not by either CD4+ or CD8+ T cells alone [2]. Macrophages are the only phagocytic cells detected in pancreatic lesions in the resulting diabetic animals. Macrophages seem to play a role in /%cell destruction as disease development can be inhibited by treatment of NOD mice with silica or antibodies directed towards the CR3 receptor on these cells [ 3 ] , and these treatments inhibit phagocytosis or binding, respectively. As in man, the disease in the NOD mouse has been shown to be under polygenic control with at least one gene linked to the class I1 region of the major histocompatibility complex (MHC). The NOD mouse has unusual features in the MHC class I1 region. This animal does not express I-E antigens because of a deletion in the promoter region of I-Ea and the sequence of its I-Ap is unique [4, 51. Analysis of DQ /3-chain (human homologue of murine I-AB) sequences in man suggested that the presence of an aspartic acid at position 57 conferred resistance to the development of IDDM [6]. As the I-@ chain of most mouse strains encodes an aspartate at position 57, whereas the NOD I-AB has a serine at this position, it was suggested that this amino acid residue might also be of importance in