| First Author | Miller AT | Year | 2002 |
| Journal | J Immunol | Volume | 168 |
| Issue | 5 | Pages | 2163-72 |
| PubMed ID | 11859102 | Mgi Jnum | J:74774 |
| Mgi Id | MGI:2159081 | Doi | 10.4049/jimmunol.168.5.2163 |
| Citation | Miller AT, et al. (2002) Defective Fas ligand expression and activation-induced cell death in the absence of IL-2-inducible T cell kinase. J Immunol 168(5):2163-72 |
| abstractText | The Tec family tyrosine kinase, IL-2-inducible T cell kinase (Itk), plays an important role in TCR signaling. Studies of T cells from Itk-deficient mice have demonstrated that Itk is critical for the activation of phospholipase-Cgamma1, leading to calcium mobilization in response to TCR stimulation. This biochemical defect results in reduced IL-2 production by Itk-deficient T cells. To further characterize the downstream effects of the Itk deficiency, we crossed Itk-/- mice to a TCR-transgenic line and examined T cell responses to stimulation by peptide plus APC. These studies show that Itk is required for maximal activation of early growth responses 2 and 3 and Fas ligand transcription after TCR stimulation. These transcriptional defects lead to reduced activation-induced cell death of stimulated Itk-/- T cells, both in vitro and in vivo. Together these studies define an important role for Itk in TCR signaling, leading to cytokine gene expression and activation-induced cell death. |
