The Journal of Experimental Medicine
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Published 15 April 2002. doi:10.1084/jem.20011435
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© Rockefeller University Press, 0022-1007/2002/4/1079/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 8, April 15, 2002 1079-1085

Brief Definitive Report

Interleukin 4 Reduces Expression of Inhibitory Receptors on B Cells and Abolishes CD22 and Fc{gamma}RII-mediated B Cell Suppression

Elizabeth U. Rudge, Antony J. Cutler, Nicholas R. Pritchard and Kenneth G.C. Smith

Cambridge Institute for Medical Research and the Department of Medicine, Wellcome Trust/MRC Building, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge CB2 2XY, United Kingdom

Address correspondence to Dr. Kenneth G.C. Smith, Cambridge Institute for Medical Research and the Department of Medicine, Wellcome Trust/MRC Building, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Hills Rd., Cambridge CB2 2XY, UK. Phone: 44-1223-762645; Fax: 44-1223-762640; E-mail: kgcs2{at}cam.ac.uk

Inhibitory receptors CD22, Fc{gamma}RII (CD32), CD72, and paired immunoglobulin-like receptor (PIR)-B are critically involved in negatively regulating the B cell immune response and in preventing autoimmunity. Here we show that interleukin 4 (IL-4) reduces expression of all four on activated B cells at the level of messenger RNA and protein. This reduced expression is dependent on continuous exposure to IL-4 and is mediated through Stat6. Coligation of Fc{gamma}RII to the B cell receptor (BCR) via intact IgG increases the B cell activation threshold and suppresses antigen presentation. IL-4 completely abolishes these negative regulatory effects of Fc{gamma}RII. CD22 coligation with the BCR also suppresses activation — this suppression too is abolished by IL-4. Thus, IL-4 is likely to enhance the B cell immune response by releasing B cells from inhibitory receptor suppression. By this coordinate reduction in expression of inhibitory receptors, and release from CD22 and Fc{gamma}RII-mediated inhibition, IL-4 is likely to play a role in T cell help of B cells and the development of T helper cell type 2 responses. Conversely, B cell activation in the absence of IL-4 would be more difficult to achieve, contributing to the maintenance of B cell tolerance in the absence of T cell help.

Key Words: interleukin 4 • B cells • CD22 • Fc{gamma}RII • inhibitory receptors


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