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Altered Neutrophil Function Induced by Serum from Patients with Systemic Lupus Erythematosus

  • G. W. Notani
  • A. J. Kenyon
  • R. B. Zurier
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 73B)

Abstract

Systemic lupus erythematosus (SLE) is a disease characterized by immunoglobulin deposition and inflammation in several organs (1). It is not clear whether these deposits, presumably in the form of immune complexes, are ingested and/or degraded by phagocytic cells. Uptake and “processing” of antigen by phagocytic cells appear necessary for lymphocytes to respond to antigen (14). Thus defects in cell mediated immunity which have been demonstrated in patients with SLE (1,9,11) may be due, in part, to defects in phagocytosis. Although leukocytes from patients with SLE exhibit impaired phagocytic activity (4), other factors have been implicated to explain the decrease in this cellular function. Thus a decrease in IgM antibody titers to bacterial antigens (2), leukopenia (13) and low levels in serum of critical complement components (16) might account for impaired phagocytosis. Recent in vitro studies have indicated the presence of a factor(s) in sera from patients with SLE which suppresses the phagocytic function of normal macrophages (18) and neutrophils (20). In the neutrophil studies, only some of the SLE sera were tested in the presence of autologous serum.

Keywords

Systemic Lupus Erythematosus Systemic Lupus Erythematosus Patient Suppressor Activity Enzyme Release Autologous Serum 
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

© Plenum Press, New York 1976

Authors and Affiliations

  • G. W. Notani
    • 1
  • A. J. Kenyon
    • 1
  • R. B. Zurier
    • 1
  1. 1.Memorial Sloan-Kettering Cancer CenterNew YorkUSA

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