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Brief Definitive Reports

Kenneth G.C. Smith^*, David M. Tarlinton, Gina M. Doody^*, Margaret L. Hibbs, and Douglas T. Fearon^*

From the ^* Wellcome Trust Immunology Unit, Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, England CB2 2SP; the Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Parkville, Victoria 3050, Australia; and the Ludwig Institute for Cancer Research, Tumour Biology Branch, Royal Melbourne Hospital, Victoria 3050, Australia

Mice in which the Lyn, Cd22, or Shp-1 gene has been disrupted have hyperactive B cells and autoantibodies. We find that in the absence of Lyn, the ability of CD22 to become tyrosine phosphorylated after ligation of mIg, to recruit SHP-1, and to suppress mIg-induced elevation of intracellular [Ca²⁺] is lost. Therefore, Lyn is required for the SHP-1–mediated B cell suppressive function of CD22, accounting for similarities in the phenotypes of these mice.

This work was supported by the Wellcome Trust through a Principal Research Fellowship (to D.T. Fearon) and a Biomedical Research Collaboration Grant (to K.G.C. Smith and D.M. Tarlinton). Additional support was provided by Grant AI-03958 from the National Institute of Allergy and Infectious Diseases (National Institutes of Health, Rockville, MD, to D.M Tarlinton), a Royal Society Project Grant (to K.G.C. Smith), a Don and Lorraine Jacquot Traveling Fellowship of the Australian and New Zealand Society of Nephrology (to K.G.C. Smith), and a Senior Research Fellowship of the Australian Research Council (to M.L. Hibbs).

Address correspondence to D.T. Fearon, Wellcome Trust Immunology Unit, Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, England CB2 2SP. Phone: 44-1223-330528; Fax: 44-1223-336815; E-mail: dtf1000{at}cus.cam.ac.uk

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This article has been cited by other articles:

• O'Keefe, T. L., Williams, G. T., Batista, F. D., Neuberger, M. S. (1999). Deficiency in CD22, a B Cell-specific Inhibitory Receptor, Is Sufficient to Predispose to Development of High Affinity Autoantibodies. JEM 189: 1307-1313 [Abstract] [Full Text]  

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