| First Author | Spain LM | Year | 1999 |
| Journal | J Immunol | Volume | 163 |
| Issue | 5 | Pages | 2681-7 |
| PubMed ID | 10453009 | Mgi Jnum | J:57089 |
| Mgi Id | MGI:1343668 | Doi | 10.4049/jimmunol.163.5.2681 |
| Citation | Spain LM, et al. (1999) T cell development in PU.1-deficient mice. J Immunol 163(5):2681-7 |
| abstractText | These studies address the role of PU.1 in T cell development through the analysis of PU.1-/- mice. We show that the majority of PU.1-/- thymocytes are blocked in differentiation prior to T cell commitment, and contain a population of thymocyte progenitors with the cell surface phenotype of CD44+, HSAbright, c-kitint, Thy-1-, CD25-, Sca-1-, CD4-, and CD8-. These cells correspond in both number and cell surface phenotype with uncommitted thymocyte progenitors found in wild-type fetal thymus. RT-PCR analysis demonstrated that PU.1 is normally expressed in this early progenitor population, but is down-regulated during T cell commitment. Rare PU.1-/- thymi, however, contained small numbers of thymocytes expressing markers of T cell commitment. Furthermore, almost 40% of PU.1-/- thymi placed in fetal thymic organ culture are capable of T cell development. Mature PU. 1-/- thymocytes generated during organ culture proliferated and produced IL-2 in response to stimulation through the TCR. These data demonstrate that PU.1 is not absolutely required for T cell development, but does play a role in efficient commitment and/or early differentiation of most T progenitors. |
