A crucial role for the p110δ subunit of phosphatidylinositol 3-kinase in B cell development and activation
The Journal of experimental medicine, 2002•rupress.org
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 …
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 …
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.
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