T cell receptor beta diversity and joining segments in the NOD mouse

Pancreatic beta-cell autoantigen recognition by the immune system appears to be a critical event in the evolution of insulin dependent diabetes. Immune recognition involves antigen presentation by macrophages and subsequent antigen-peptide-class II MHC recognition by T cell receptors (TCR). Using the NOD mouse as a model for human IDD, we hypothesized that germline variability in the D beta nod and/or J beta nod segments could contribute to beta cell autoimmunity by influencing the specific peptides that are recognized. As an initial approach to our hypothesis, we sought to compare these segments to other strains of mice in search of genetic polymorphisms as reported in NZW mice. The germ line TCR beta nod gene did not display evidence of an expansion or contraction in the number of D beta nod or J beta nod segments at the level of resolution provided by restriction fragment length polymorphism analysis. The absence of such polymorphisms suggests that D beta nod or J beta nod segments are not different from nonautoimmune strains of mice.