| First Author | Liao XC | Year | 1997 |
| Journal | J Exp Med | Volume | 186 |
| Issue | 12 | Pages | 2069-73 |
| PubMed ID | 9396778 | Mgi Jnum | J:44879 |
| Mgi Id | MGI:1101425 | Doi | 10.1084/jem.186.12.2069 |
| Citation | Liao XC, et al. (1997) Itk and Fyn make independent contributions to T cell activation. J Exp Med 186(12):2069-73 |
| abstractText | Itk is a member of the Btk/Tec/Itk family of nonreceptor protein tyrosine kinases (PTKs), and has been implicated in T cell antigen receptor (TCR) signal transduction. Lck and Fyn are the Src-family nonreceptor PTKs that are involved in TCR signaling. To address the question of how these members of different families of PTKs functionally contribute to T cell development and to T cell activation, mice deficient for both Itk and either Lck or Fyn were generated. The Itk/Lck doubly deficient mice exhibited a phenotype similar to that of Lck-deficient mice. The phenotype of the Itk/Fyn doubly deficient mice was similar to that of Itk deficient mice. However the Itk/Fyn doubly deficient mice exhibited a more severe defect in TCR-induced proliferation of thymocytes and peripheral T cells than did mice deficient in either kinase alone. These data support the notion that Itk and Fyn both make independent contributions to TCR-induced T cell activation. |
