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Altered Expression of Fcγ and Complement Receptors on B Cells in Systemic Lupus Erythematosus
Author(s) -
GERGELY PÉTER,
ISAÁK ANDREA,
SZEKERES ZSUZSANNA,
PRECHL JÓZSEF,
ERDEI ANNA,
NAGY ZSOLT B.,
GERGELY JÁNOS,
POÓR GYULA
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1422.020
Subject(s) - receptor , autoantibody , immunology , immune receptor , pathogenesis , complement receptor , systemic lupus erythematosus , complement system , lupus erythematosus , immune system , b cell , biology , autoimmune disease , antibody , medicine , disease , genetics
Abstract : 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.