부산대학교 도서관

A congenic, non-obese diabetic (NOD) mouse strain that contains a segment of chromosome 3 from the diabetes-resistant mouse strain B6.PL-Thy-[1.sup.a] was less susceptible to diabetes than NOD mice. A fully penetrant immunological defect also mapped to this segment, which encodes the high-affinity Fc receptor for immunoglobulin G (IgG), FcγRI. The NOD Fcgr1 allele, which results in a deletion of the cytoplasmic tail, caused a 73 percent reduction in the turnover of cell surface receptor-antibody complexes. The development of congenic strains and the characterization of Mendelian traits that are specific to the disease phenotype demonstrate the feasibility of dissecting the pathophysiology of complex, non-Mendelian diseases.
Complex diseases such as autoimmune, insulin-dependent diabetes mellitus (IDDM) [1-4], hypertension[5], and epilepsy[6] are largely determined by a number of gene effects. The NOD mouse strain spontaneously develops IDDM[7], which [...]