Complement-Dependent Alterations in the Handling of Immune Complexes by NZB/W Mice

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Abstract
Serum of normal mammals contains factors which can release antigen-antibody complexes from the surfaces of leukocytes and platelets. This “complex release activity” (CRA) is mediated by the alternative pathway of complement activation, and is measured by a kinetic assay of the release of lymphocyte-bound soluble immune complexes. CRA activity was measured in the sera of NZB/W mice, which develop an autoimmune disease with aging. CRA in these mice declined rapidly after 16 weeks of age, and by 32 weeks was barely detectable. Serum C3 levels also declined in these mice. An association test correlating CRA and C3 concentration was highly significant. The decreased complement levels in the older mice led to profound changes in their handling of injected soluble immune complexes, as demonstrated in studies of the kinetics of distribution of the complexes between plasma and circulating cells. These abnormalities may be related to the disease which occurs spontaneously in NZB/W mice, as well as in human immune complex diseases.

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