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Science 30 April 1993:
Vol. 260. no. 5108, pp. 695 - 698
DOI: 10.1126/science.8480181
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Articles

Science, Vol 260, Issue 5108, 695-698
Copyright © 1993 by American Association for the Advancement of Science

articles

Linkage on chromosome 3 of autoimmune diabetes and defective Fc receptor for IgG in NOD mice

JB Prins, JA Todd, NR Rodrigues, S Ghosh, PM Hogarth, LS Wicker, E Gaffney, PL Podolin, PA Fischer, A Sirotina, and al. et

Nuffield Department of Surgery, University of Oxford, John Radcliffe Hospital, Headington, United Kingdom.

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), Fc gamma RI. 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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