Altered Expression of Fcγ and Complement Receptors on B Cells in Systemic Lupus Erythematosus

Authors: GERGELY, PÉTER; ISAÁK, ANDREA1; SZEKERES, ZSUZSANNA1; PRECHL, JÓZSEF1; ERDEI, ANNA; NAGY, ZSOLT B.; GERGELY, JÁNOS; POÓR, GYULA

Source: Annals of the New York Academy of Sciences, Volume 1108, Number 1, June 2007 , pp. 183-192(10)

Publisher: Blackwell Publishing

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Abstract:

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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by B cell hyper-reactivity, autoantibody production, immune complex (IC) deposition, and multiple organ damage. The contribution of IC and B cell-mediated changes in the pathogenesis of SLE is well established, however, the exact role of IC-binding receptors expressed on B cells, Fcγ receptors, and complement receptors CR1 and CR2 in these pathological processes is unclear. Development of lupus-like symptoms in mice defective for the inhibitory FcγRIIb and genetic association of certain FcγR genes with SLE demonstrate a significant role for these receptors but reports indicating alterations of Fcγ or complement receptor-mediated B cell functions in human SLE are relatively few. The present review highlights a selected set of data including our own discussing the significance of animal models, genetics, and functional alterations of these IC-binding receptors in the etiopathogenesis of SLE.

Keywords: B cell; Fcγ receptor; complement receptor; SLE

Document Type: Research article

DOI: 10.1196/annals.1422.020

Affiliations: 1: Department of Immunology, Eötvös Loránd University, Pázmány Péter s. 1/C, Budapest H-1117, Hungary

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