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 language | English |
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Pages (from-to) | 753-763 |
Number of pages | 11 |
Journal | Journal of Experimental Medicine |
Volume | 196 |
Issue number | 6 |
DOIs | |
Publication status | Published - 9 Sept 2002 |
Keywords
- Akt
- Btk
- Calcium
- Gene targeting
- p110δ
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology