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Activation FcyR Are Required for the Development of Tissue Pathology in Autoimmune Glomerulonephritis

A spontaneous model of lupus, the NZBxNZW f1, develops fatal glomerulonephritis as a consequence of immune complex deposition in the kidney. Deletion of the activation FcR g chain protects this susceptible strain from inflammatory disease, while not affecting immune complex deposition or C3 deposition. Complement C3 is insufficient to trigger inflammation in the absence of activation FcRs, demonstrating the critical role of these receptors in coupling IgG antibodies to inflammatory pathways. Activation FcRs are thus attractive targets for modulating inflammation in autoimmune diseases like lupus and rheumatoid arthritis.

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