volume 186, issue 5, P777-783 1997
DOI: 10.1084/jem.186.5.777
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Abstract: Recent understanding of the mechanism of immunoglobulin G (IgG) catabolism has yielded new insight into antibody-mediated diseases. We proposed that β2-microglobulin (β2m)–deficient mice have been protected from systemic lupus erythematosis (SLE)–like syndromes because they lack the β2m-associated IgG protection receptor (FcRn) and therefore catabolize IgG, including pathogenic IgG autoantibodies, considerably more rapidly than normal mice. Such an hypothesis would predict that β2m-deficient mice would also be…

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