LINKAGE ON CHROMOSOME-3 OF AUTOIMMUNE DIABETES AND DEFECTIVE FC RECEPTOR FOR IGG IN NOD MICE

A congenic, non-obese diabetic (NOD) mouse strain that contains a segm ent of chromosome 3 from the diabetes-resistant mouse strain B6.PL-Thy -1a was less susceptible to diabetes than NOD mice. A fully penetrant immunological defect also mapped to this segment, which encodes the hi gh-affinity Fc receptor for immunoglobulin G (IgG), FcgammaRI. The NOD Fcgr1 allele, which results in a deletion of the cytoplasmic tail, ca used a 73 percent reduction in the turnover of cell surface receptor-a ntibody complexes. The development of congenic strains and the charact erization of Mendelian traits that are specific to the disease phenoty pe demonstrate the feasibility of dissecting the pathophysiology of co mplex, non-Mendelian diseases.