| First Author | Hagenbeek TJ | Year | 2004 |
| Journal | J Exp Med | Volume | 200 |
| Issue | 7 | Pages | 883-94 |
| PubMed ID | 15452180 | Mgi Jnum | J:93376 |
| Mgi Id | MGI:3056957 | Doi | 10.1084/jem.20040495 |
| Citation | Hagenbeek TJ, et al. (2004) The Loss of PTEN Allows TCR {alpha}{beta} Lineage Thymocytes to Bypass IL-7 and Pre-TCR-mediated Signaling. J Exp Med 200(7):883-894 |
| abstractText | The phosphatase and tensin homologue deleted on chromosome 10 (PTEN) negatively regulates cell survival and proliferation mediated by phosphoinositol 3 kinases. We have explored the role of the phosphoinositol(3,4,5)P3-phosphatase PTEN in T cell development by analyzing mice with a T cell-specific deletion of PTEN. Pten(flox/flox)Lck-Cre mice developed thymic lymphomas, but before the onset of tumors, they showed normal thymic cellularity. To reveal a regulatory role of PTEN in proliferation of developing T cells we have crossed PTEN-deficient mice with mice deficient for interleukin (IL)-7 receptor and pre-T cell receptor (TCR) signaling. Analysis of mice deficient for Pten and CD3gamma; Pten and gammac; or Pten, gammac, and Rag2 revealed that deletion of PTEN can substitute for both IL-7 and pre-TCR signals. These double- and triple-deficient mice all develop normal levels of CD4CD8 double negative and double positive thymocytes. These data indicate that PTEN is an important regulator of proliferation of developing T cells in the thymus. |
