A crucial role for the p110δ subunit of phosphatidylinositol 3-kinase in B cell development and activation

Elizabeth Clayton, Giuseppe Bardi, Sarah E. Bell, David Chantry, Charles Downes, Alexander Gray, Lisa A. Humphries, David Rawlings, Helen Reynolds, Elena Vigorito, Martin Turner

    Research output: Contribution to journalArticlepeer-review

    358 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)753-763
    Number of pages11
    JournalJournal of Experimental Medicine
    Volume196
    Issue number6
    DOIs
    Publication statusPublished - 9 Sep 2002

    Keywords

    • Akt
    • Btk
    • Calcium
    • Gene targeting
    • p110δ

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