| First Author | Jabeen R | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 7 | Pages | e22189 |
| PubMed ID | 21779390 | Mgi Jnum | J:175789 |
| Mgi Id | MGI:5287323 | Doi | 10.1371/journal.pone.0022189 |
| Citation | Jabeen R, et al. (2011) The transcription factor PU.1 regulates gammadelta T cell homeostasis. PLoS One 6(7):e22189 |
| abstractText | BACKGROUND: T cell development results in the generation of both mature alphabeta and gammadelta T cells. While alphabeta T cells predominate in secondary lymphoid organs, gammadelta T cells are more abundant in mucosal tissues. PU.1, an Ets family transcription factor, also identified as the spleen focus forming virus proviral integration site-1 (Sfpi1) is essential for early stages of T cell development, but is down regulated during the DN T-cell stage. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we show that in mice specifically lacking PU.1 in T cells using an lck-Cre transgene with a conditional Sfpi1 allele (Sfpi1(lck-/-)) there are increased numbers of gammadelta T cells in spleen, thymus and in the intestine when compared to wild-type mice. The increase in gammadelta T cell numbers in PU.1-deficient mice is consistent in gammadelta T cell subsets identified by TCR variable regions. PU.1-deficient gammadelta T cells demonstrate greater proliferation in vivo and in vitro. CONCLUSIONS/SIGNIFICANCE: The increase of gammadelta T cell numbers in Lck-Cre deleter strains, where deletion occurs after PU.1 expression is diminished, as well as the observation that PU.1-deficient gammadelta T cells have greater proliferative responses than wild type cells, suggests that PU.1 effects are not developmental but rather at the level of homeostasis. Thus, our data shows that PU.1 has a negative influence on gammadelta T cell expansion. |
