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2-microglobulin-deficient Mice Are Resistant to
Bullous Pemphigoid
By
From the * Department of Dermatology, Medical College of Wisconsin, Milwaukee, Wisconsin 43226; Recent understanding of the mechanism of immunoglobulin G (IgG) catabolism has yielded
new insight into antibody-mediated diseases. We proposed that The Jackson Laboratory, Bar Harbor, Maine 04609; and the § Department of Internal Medicine and
the Department of Pathology, The Ohio State University, Columbus, Ohio 43210
2-microglobulin (2m)-deficient mice have been protected from systemic lupus erythematosis (SLE)-like syndromes because they lack the 2m-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 2m-deficient mice would also be resistant to experimental bullous pemphigoid, a disease with a pathogenesis thought to be much simpler than
SLE, being the result of antibody directed toward a pathogenic epitope on the epidermal
hemidesmosome that anchors basal keratinocytes to the basement membrane. To test this hypothesis, we administered pathogenic rabbit antibody directed toward the hemidesmosome to 2m-deficient mice and to normal control mice, both intraperitoneally and intradermally, and
assessed the mice clinically, histologically, and immunologically for manifestations of skin disease. We found that the 2m-deficient mice were protected when the antibody was given intraperitoneally whereas intradermal administration resulted in blisters only slightly less severe
than those seen in normal mice. These data would indicate that autoantibody-mediated inflammation might be prevented or controlled by appropriate modulation of FcRn function.
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