| First Author | Thomis DC | Year | 1997 |
| Journal | J Exp Med | Volume | 185 |
| Issue | 2 | Pages | 197-206 |
| PubMed ID | 9016869 | Mgi Jnum | J:128694 |
| Mgi Id | MGI:3767851 | Doi | 10.1084/jem.185.2.197 |
| Citation | Thomis DC, et al. (1997) Peripheral expression of Jak3 is required to maintain T lymphocyte function. J Exp Med 185(2):197-206 |
| abstractText | The Jak family tyrosine kinase, Jak3, is involved in signaling through cytokine receptors that utilize the common gamma chain (gammac), such as those for IL-2, IL-4, IL-7, IL-9, and IL-15. Recent studies of Jak3-deficient mice and humans have demonstrated that Jak3 plays a critical role in B and T lymphocyte maturation and function. The T lymphocyte defects in Jak3-deficient mice include a small thymus, a decrease in peripheral CD8+ cells, an increase in the surface expression of activation markers, and a severe reduction in proliferative and cytokine secretion responses to mitogenic stimuli. To determine whether the peripheral T lymphocyte defects result from aberrant maturation in the thymus or from the absence of Jak3 protein in peripheral T cells, we generated reconstituted mice that express normal levels of Jak3 protein in the thymus but lose Jak3 expression in peripheral T cells. Jak3 expression in the thymus restores normal T cell development, including CD8+, gammadelta, and natural killer cells. However, the loss of Jak3 protein in peripheral T cells leads to the Jak3-/- phenotype, demonstrating that Jak3 is constitutively required to maintain T cell function. |
