Altered expression of Fcgamma and complement receptors on B cells in systemic lupus erythematosus.
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, Fcgamma receptors, and complement receptors CR1 and CR2 in these pathological processes is unclear. Development of lupus-like symptoms in mice defective for the inhibitory Fc-gammaRIIb and genetic association of certain FcgammaR genes with SLE demonstrate a significant role for these receptors but reports indicating alterations of Fcgamma 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.
Gergely
Péter
P
National Institute of Rheumatology and Physiotherapy, Frankel Leo u. 25-29, Budapest H-1023, Hungary. gergelypeter@orfi.hu
Isaák
Andrea
A
Szekeres
Zsuzsanna
Z
Prechl
József
J
Erdei
Anna
A
Nagy
Zsolt B
ZB
Gergely
János
J
Poór
Gyula
G
D000818:Animals; D000936:Antigen-Antibody Complex; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000276:immunology / Q000378:metabolism*; D051379:Mice; D011951:Receptors, Complement / Q000096:biosynthesis* / Q000276:immunology; D017452:Receptors, IgG / Q000096:biosynthesis* / Q000276:immunology
D000936:Antigen-Antibody Complex; D011951:Receptors, Complement; D017452:Receptors, IgG