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Volume 187, Issue 5
2 March 1998
Journal of Experimental Medicine Cover Image for Volume 187, Issue 5
Article Contents
Brief Definitive Report| March 02 1998

Inhibition of the B Cell by CD22: A Requirement for Lyn

Kenneth G.C. Smith,
Kenneth G.C. Smith
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
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David M. Tarlinton,
David M. Tarlinton
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
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Gina M. Doody,
Gina M. Doody
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
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Margaret L. Hibbs,
Margaret L. Hibbs
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
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Douglas T. Fearon
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
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Author and Article Information
Kenneth G.C. Smith, David M. Tarlinton, Gina M. Doody, Margaret L. Hibbs, 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

We thank Amanda Light for expert technical assistance.

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: [email protected]

Received: November 21 1997
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1998
J Exp Med (1998) 187 (5): 807–811.
https://doi.org/10.1084/jem.187.5.807
Article history
Received:
November 21 1997

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.

1998
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