A Crucial Role for the p110δ Subunit of Phosphatidylinositol 3-Kinase in B Cell Development and Activation

DOI PDF 9 Citations
  • Elizabeth Clayton
    1Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, United Kingdom
  • Giuseppe Bardi
    1Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, United Kingdom
  • Sarah E. Bell
    1Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, United Kingdom
  • David Chantry
    2COS Corporation, Bothell, WA 98021
  • C. Peter Downes
    3Department of Biochemistry, University of Dundee, Dundee, DD1 5EH, United Kingdom
  • Alexander Gray
    3Department of Biochemistry, University of Dundee, Dundee, DD1 5EH, United Kingdom
  • Lisa A. Humphries
    4The Molecular Biology Institute, University of California, Los Angeles, CA 90095
  • David Rawlings
    5Department of Immunology, University of Washington, School of Medicine, Seattle, WA 98195
  • Helen Reynolds
    1Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, United Kingdom
  • Elena Vigorito
    1Laboratory of Lymphocyte Signaling and Development, Molecular Immunology Programme, The Babraham Institute, Babraham, Cambridge CB2 4AT, United Kingdom
  • Martin Turner
    5Department of Immunology, University of Washington, School of Medicine, Seattle, WA 98195

Description

<jats:p>Mice lacking the p110δ catalytic subunit of phosphatidylinositol 3-kinase have reduced numbers of B1 and marginal zone B cells, reduced levels of serum immunoglobulins, respond poorly to immunization with type II thymus-independent antigen, and are defective in their primary and secondary responses to thymus-dependent antigen. p110δ−/− B cells proliferate poorly in response to B cell receptor (BCR) or CD40 signals in vitro, fail to activate protein kinase B, and are prone to apoptosis. p110δ function is required for BCR-mediated calcium flux, activation of phosphlipaseCγ2, and Bruton's tyrosine kinase. Thus, p110δ plays a critical role in B cell homeostasis and function.</jats:p>

Journal

Citations (9)*help

See more

Details 詳細情報について

Report a problem

Back to top