An abnormality of the gene that encodes neutrophil Fc receptor III in a patient with systemic lupus erythematosus.

M R Clark; L Liu; S B Clarkson; P A Ory; I M Goldstein

doi:10.1172/JCI114706

Rosalind Russell Arthritis Research Laboratory, Department of Medicine, University of California, San Francisco 94143.

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Rosalind Russell Arthritis Research Laboratory, Department of Medicine, University of California, San Francisco 94143.

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Rosalind Russell Arthritis Research Laboratory, Department of Medicine, University of California, San Francisco 94143.

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Rosalind Russell Arthritis Research Laboratory, Department of Medicine, University of California, San Francisco 94143.

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Rosalind Russell Arthritis Research Laboratory, Department of Medicine, University of California, San Francisco 94143.

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Published in Volume 86, Issue 1 on July 1, 1990
J Clin Invest. 1990;86(1):341–346. https://doi.org/10.1172/JCI114706.
© 1990 The American Society for Clinical Investigation

Published July 1, 1990 - Version history

In the course of examining the structure and function of Fc receptors on peripheral blood cells of patients with systemic lupus erythematosus, we identified a patient whose neutrophils did not react with either monoclonal or polyclonal antibodies to Fc receptor III. However, neutrophils from the patient were comparable to neutrophils from healthy controls with respect to their expression of Fc receptor II, complement receptor 1, complement receptor 3, and the phosphatidylinositol-linked, complement regulatory protein, decay-accelerating factor. The abnormality of expression of Fc receptor III was limited to the patient's neutrophils (her natural killer cells reacted normally with anti-Fc receptor III antibodies), and was associated with abnormal recognition and binding of IgG-coated erythrocytes. Analysis of genomic DNA revealed evidence that failure of the patient's neutrophils to express Fc receptor III was most likely due to an abnormality of the gene that encodes this receptor.

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