| First Author | Thomis DC | Year | 1997 |
| Journal | J Immunol | Volume | 159 |
| Issue | 10 | Pages | 4708-19 |
| PubMed ID | 9366394 | Mgi Jnum | J:43961 |
| Mgi Id | MGI:1099212 | Doi | 10.4049/jimmunol.159.10.4708 |
| Citation | Thomis DC, et al. (1997) T cells from Jak3-deficient mice have intact TCR signaling, but increased apoptosis. J Immunol 159(10):4708-19 |
| abstractText | The Jak family tyrosine kinase, Jak3, is involved in signaling through cytokine receptors utilizing the common gamma-chain (gamma(c)). Mice and humans lacking Jak3 have severe immune deficiencies, including defects in B and T lymphocyte development and function. In particular, Jak3-deficient mice have mature T cells with an activated phenotype, yet these cells are functionally nonresponsive. In this work, we show that Jak3-deficient T cells have no gross defects in early T cell signaling, as measured by TCR-induced tyrosine phosphorylation and calcium mobilization responses. Furthermore, we find that Jak3-deficient mice expressing a transgenic TCR have extremely low numbers of peripheral T cells with a naive phenotype, indicating that both peripheral activation and expansion of Jak3-/- T cells are driven by antigenic signals. We show that, similar to gamma(c)-deficient mice, T cells from Jak3-deficient mice have an increased susceptibility to apoptosis. Previously, we showed that when stimulated in vitro by CD3 plus CD28 cross-linking, Jak3-/- T cells secrete greatly reduced amounts of IL-2, and fail to proliferate. However, by measuring intracellular IL-2 levels, we find that Jak3-/- T cells produce amounts of IL-2 similar to activated T cells from control mice, further supporting the notion that there is no defect in TCR signaling in Jak3-/- T cells. |
