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Abstract
Phosphoinositide kinase (PI3K) is activated by various receptors on lymphocytes and regulates development, activation, and tolerance. Genetic ablation of PI3K function in T cells leads to the appearance of autoimmune disorders. In B cells, loss of the class IA regulatory subunit p85α causes a partial defect in B cell development and proliferation, whereas loss of p85β alone causes no apparent changes in B cell function. Here we investigate further the consequences of p85β deletion in B cells, in the presence or absence of p85α. We demonstrate that p85β partially compensates for loss of p85α in B cell development and peripheral survival, with greater defects observed when both isoforms are absent. BCR-mediated AKT phosphorylation is partially reduced in p85α-deficient B cells and further diminished with concomitant loss of p85β. Unexpectedly, loss of p85β results in increased BCR-mediated proliferation and ERK phosphorylation. These results indicate that the p85β regulatory isoform has partially overlapping functions with p85α in B cells as well as a unique role in opposing BCR responses.
| Abbreviations | ||
| PI3K | = | phosphoinositide 3-kinase |
| PtdIns | = | phosphatidylinositol |
| mTOR | = | mammalian target of rapamycin |
| WT | = | wild-type |
| KO | = | knockout |
| Abbreviations | ||
| PI3K | = | phosphoinositide 3-kinase |
| PtdIns | = | phosphatidylinositol |
| mTOR | = | mammalian target of rapamycin |
| WT | = | wild-type |
| KO | = | knockout |