The Journal of Experimental Medicine
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Published online March 24, 2008
doi:10.1084/jem.20072565
The Journal of Experimental Medicine, Vol. 205, No. 4, 883-895
The Rockefeller University Press, 0022-1007 $30.00
© 2008 Brownlie et al.
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ARTICLE

 Distinct cell-specific control of autoimmunity and infection by Fc{gamma}RIIb

Rebecca J. Brownlie1, Kate E. Lawlor1, Heather A. Niederer1, Antony J. Cutler1, Zou Xiang1, Menna R. Clatworthy1, R. Andres Floto1, David R. Greaves2, Paul A. Lyons1, and Kenneth G.C. Smith1

1 Cambridge Institute for Medical Research and the Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge CB2 2OY, England, UK
2 Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK

CORRESPONDENCE Kenneth G.C. Smith: kgcs2{at}cam.ac.uk

Fc{gamma}RIIb 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 Fc{gamma}RIIb can modulate these processes, we created transgenic mice overexpressing Fc{gamma}RIIb on B cells or macrophages. Overexpression of Fc{gamma}RIIb 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 Fc{gamma}RIIb in immune responses, demonstrate the contrasting roles played by Fc{gamma}RIIb on B cells and macrophages in the control of infection and autoimmunity, and emphasize the therapeutic potential for modulation of Fc{gamma}RIIb expression on B cells in inflammatory and autoimmune disease.

Abbreviations used: ANA, antinuclear antibodies; B-NTG and -TG, B cell nontransgenic and transgenic, respectively; CGG, chicken {gamma} globulin; CIA, collagen-induced arthritis; CII, type II collagen; ERK, extracellular signal-regulated kinase; FDC, follicular dendritic cell; GC, germinal center; M-NTG and -TG, macrophage nontransgenic and transgenic, respectively; NP, 4-hydroxyl-3-nitrophenyl acetyl; PC, phosphorylcholine; SLE, systemic lupus erythematosus.

A.J. Cutler's present address is Histocompatibility and Immunogenetics, NHS Blood and Transplant, Colindale Centre, London NW9 5BG, England, UK.

R.A. Floto's present address is Cystic Fibrosis and Lung Defence Unit, Papworth Hospital NHS Foundation Trust, Cambridge CB23 3RE, England, UK.


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