RES impairment in NZB/W mice
NZBAV mice develop a murine lupus very similar to human systemic lupus erythematosus (SLE). The pathogenesis of both diseases remains poorly understood. There is, however, extensive evidence that antigen-antibody complexes play a central role1,2. Much of the tissue damage in these diseases appear to result from deposition of immune complexes in the kidney and other tissue3,4 and the attendant initiation of inflammatory events. Tissue localization may occur from a failure to clear immune complexes from the circulation due to (1) an excessive rate of antibody production and the consequent overloading of the reticuloendothelial system (RES), (2) a subnormal rate of catabolic removal of immune complexes due to impaired RES function, or (3) a combination of these two phenomena. Investigations in the past have placed much emphasis on the hyperactivity of autoantibody production whereas possible impairment of the disposal system for the immune complexes has not received due attention. This investigation was conducted to ascertain whether an impairment in the disposal of soluble immune complexes underlies, or at least contributes to, the pathogenesis of murine lupus in NZB/W mice.
KeywordsSystemic Lupus Erythematosus Immune Complex Peritoneal Macrophage Swiss Webster Mouse Murine Lupus
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