RES impairment in NZB/W mice

  • Y-H. Chang
  • C. M. Pearson
  • D. Chia
  • K. R. Aoki
Part of the Inflammation: Mechanisms and Treatment book series (FTIN, volume 4)


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.


Systemic Lupus Erythematosus Immune Complex Peritoneal Macrophage Swiss Webster Mouse Murine Lupus 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© MTP Press Limited 1980

Authors and Affiliations

  • Y-H. Chang
    • 1
  • C. M. Pearson
    • 1
  • D. Chia
    • 1
  • K. R. Aoki
    • 1
  1. 1.USA

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