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FcgammaRIIb is an inhibitory Fc receptor expressed on B cells and myeloid cells. It is important in controlling responses to infection, and reduced expression or function predisposes to autoimmunity. To determine if increased expression of FcgammaRIIb can modulate these processes, we created transgenic mice overexpressing FcgammaRIIb on B cells or macrophages. Overexpression of FcgammaRIIb on B cells reduced the immunoglobulin G component of T-dependent immune responses, led to early resolution of collagen-induced arthritis (CIA), and reduced spontaneous systemic lupus erythematosus (SLE). In contrast, overexpression on macrophages had no effect on immune responses, CIA, or SLE but increased mortality after Streptococcus pneumoniae infection. These results help define the role of FcgammaRIIb in immune responses, demonstrate the contrasting roles played by FcgammaRIIb on B cells and macrophages in the control of infection and autoimmunity, and emphasize the therapeutic potential for modulation of FcgammaRIIb expression on B cells in inflammatory and autoimmune disease.

Original publication

DOI

10.1084/jem.20072565

Type

Journal article

Journal

J Exp Med

Publication Date

14/04/2008

Volume

205

Pages

883 - 895

Keywords

Animals, Antigens, CD, Arthritis, Experimental, Autoimmunity, B-Lymphocytes, B7-2 Antigen, Bacterial Infections, Cell Proliferation, Extracellular Signal-Regulated MAP Kinases, Humans, Immunoglobulin G, Infection, Lupus Erythematosus, Systemic, Macrophages, Mice, Mice, Transgenic, Organ Specificity, Phosphorylation, Receptors, IgG, T-Lymphocytes, Transgenes