An early molecular event in the evolution of insulindependent diabetes in humans and NOD mice appears to involve the interaction of MHC class II molecules, β-cell autoantigen-derived peptides, and receptor molecules of helper T lymphocytes. To examine the influence of T-lymphocyte-receptor p-genes on the development of β-cell autoimmunity, (NOD × NZW)F1 × NOD backcrossed (BC) mice were studied for the development of insulitis, because insulitis is the pathognomonic histological lesion of autoimmune diabetes. Heterozygosity for H-2nod was permissive for the development of pancreatic interstitial inflammation and peri-islet insulitis, whereas homozygosity for H-2nod was highly associated with insulitis. However, (NOD × NZW)F1 × NOD BC mice developed insulitis regardless of homozygosity or heterozygosity for T-lymphocyte receptor βnod. Therefore, in our study, T-lymphocyte receptor βnod did not function as an autosomal-recessive β-cell autoimmunity gene.

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