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

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

doi:10.1084/jem.187.5.807

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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

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

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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