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Neutrophil Aggregation Induced by Sera from Patients with Active Systemic Lupus Erythematosus
Author(s) -
Abramson Steven B.,
Given William P.,
Edelson Henry S.,
Weissmann Gerald
Publication year - 1983
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780260509
Subject(s) - medicine , immunology , rheumatoid arthritis , immune system , neutropenia , in vivo , complement system , respiratory distress , immune complex , in vitro , respiratory burst , systemic lupus erythematosus , arthritis , disease , biology , toxicity , biochemistry , microbiology and biotechnology , anesthesia
Activated complement components and immune complexes cause neutrophil (PMN) aggregation in vitro and in vivo, as in dialysis‐induced neutropenia and adult respiratory distress syndrome. To investigate the possible role of PMN aggregation in systemic lupus erythematosus (SLE), we studied the capacity of 59 sera from 53 patients to induce aggregation of normal PMN in vitro. Neutrophil aggregating activity (NAA) was present in the sera of 26 of 28 patients with active SLE. The mean NAA in this group was significantly greater than that found in 13 patients with inactive SLE, 20 patients with rheumatoid arthritis, and 17 normal controls. In patients with SLE there was a positive correlation between disease severity and the quantitative measure of NAA. NAA did not correlate with serum C3 or C4 nor with the presence or absence of circulating immune complexes. High levels of NAA were particularly characteristic of central nervous system lupus. These data suggest that the formation of intravascular leukoaggregates may contribute to morbidity in SLE.

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