Linkage on chromosome 3 of autoimmune diabetes and defective Fc receptor for IgG in NOD mice
Science, 1993•science.org
A congenic, non-obese diabetic (NOD) mouse strain that contains a segment 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 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 …
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 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 …
A congenic, non-obese diabetic (NOD) mouse strain that contains a segment 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 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.
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