ABSTRACT
Type I diabetes of man, the BB rat and the nonobese diabetic (NOD) mouse appears to result from autoimmune beta cell destruction in the setting of a genetic predisposition. This chapter summarizes the immunogenetics and immunopathogenesis of the NOD mouse. Initial breeding studies by Makino and co-workers3,5 in crosses of NOD with control C57BL/6 mice suggest that insulitis of the NOD mouse is regulated by two autosomal recessive genes. Several pieces of evidence indicate that beta cell destruction of the NOD mouse is of autoimmune origin. First, the disease can be adoptively transferred with lymphoid cells from NOD mice. Second, diabetes of the NOD mouse can be either enhanced or prevented by several immunological manipulations. Development of diabetes of the NOD mouse is regulated by at least three autosomal recessive genes. These genes, in addition to environmental factors and immunological predisposition, lead to the development of diabetes.
