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Fcγ Receptor Polymorphisms

Insights into Pathogenesis

  • Chapter
Lupus

Part of the book series: Contemporary Immunology ((CONTIM))

Abstract

Two decades ago, seminal studies from the National Institute of Health identified impairment of in vivo Fc receptor specific function in patients with systemic lupus erythematosus (SLE) (1). Further work demonstrated that this receptor dysfunction correlated with immune complex levels measured by complement-independent assays (2), varied with disease activity both within individual patients and across patient cohorts (2–5), and also occurred in patients with various types of immune complex disease (6,7). Efforts to understand the molecular basis of these findings accelerated with the cloning of eight distinct genes, grouped in three highly homologous families, for human Fcγ receptors. Through intrinsic differences in each gene and through alternative splicing, these genes yield 10 or so distinct protein products (8–14).

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Authors
  1. Andrew W. Gibson
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  2. Jianming Wu
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  3. Jeffrey C. Edberg
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  4. Robert P. Kimberly
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Editors and Affiliations

  1. Section on Rheumatology, Department of Internal Medicine, The Wake Forest University School of Medicine, Winston-Salem, NC, USA

    Gary M. Kammer MD

  2. Division of Rheumatology and Immunology, Uniformed Services University of Health Sciences, Bethesda, MD, USA

    George C. Tsokos MD

  3. Department of Clinical Physiology, Walter Reed Army Institute of Research, Washington, DC, USA

    George C. Tsokos MD

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Gibson, A.W., Wu, J., Edberg, J.C., Kimberly, R.P. (1999). Fcγ Receptor Polymorphisms. In: Kammer, G.M., Tsokos, G.C. (eds) Lupus. Contemporary Immunology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-703-1_34

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  • DOI: https://doi.org/10.1007/978-1-59259-703-1_34

  • Publisher Name: Humana Press, Totowa, NJ

  • Print ISBN: 978-1-4757-5686-9

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