| First Author | Saijo K | Year | 1997 |
| Journal | J Exp Med | Volume | 185 |
| Issue | 2 | Pages | 351-6 |
| PubMed ID | 9016883 | Mgi Jnum | J:111310 |
| Mgi Id | MGI:3653581 | Doi | 10.1084/jem.185.2.351 |
| Citation | Saijo K, et al. (1997) Crucial role of Jak3 in negative selection of self-reactive T cells. J Exp Med 185(2):351-6 |
| abstractText | Jak3 mediates growth signals through cytokine receptors such as interleukin-2 (IL-2), IL-4, and IL-7, and its deficiency results in autosomal recessive SCID in mice and humans. In spite of the severely reduced number of lymphocytes in Jak3-deficient mice, the differentiation profile of thymocytes was normal and mature T cells accumulated in the periphery with age. However, we found that self-reactive T cells were not deleted in the thymus and the peripheral tissues in Jak3-deficient mice. All peripheral T cells were in the activation state and thus were unable to be activated further, as demonstrated by the failure of eliciting Ca2+ response upon T cell receptor (TCR) stimulation. From the analysis of TCR-transgenic Jak3-deficient mice, only self-reactive T cells appeared to be in the activated state and anergic. These findings demonstrate a crucial function of Jak3 in the negative selection of autoreactive T cells and the maintenance of functional peripheral T cells. |
