| First Author | Webb LM | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 5 | Pages | 2783-7 |
| PubMed ID | 16116162 | Mgi Jnum | J:113237 |
| Mgi Id | MGI:3664836 | Doi | 10.4049/jimmunol.175.5.2783 |
| Citation | Webb LM, et al. (2005) Cutting edge: T cell development requires the combined activities of the p110gamma and p110delta catalytic isoforms of phosphatidylinositol 3-kinase. J Immunol 175(5):2783-7 |
| abstractText | The role of PI3K activity in T lymphocyte development is obscure because mice deficient in single PI3K catalytic subunits either die before birth (p110alpha-/- and p110beta-/-) or lack a significant T cell developmental phenotype (p110gamma-/- and p110delta-/-). We have generated mice deficient in both p110gamma and p110delta and show that p110gamma/delta-/- mice have a profound block in T cell development that occurs at the beta-selection checkpoint. We show that pre-TCR-induced signaling is significantly reduced in p110gamma/delta-/- thymocytes and that this results in a concomitant lack of proliferative expansion and increased apoptosis. The survival defect in p110gamma/delta-/- thymocytes is associated with increased levels of the pro-apoptotic molecule Bcl2 interacting mediator of cell death. This work demonstrates that PI3K activity is critical for T cell development and depends on the combined function of p110gamma and p110delta. |
