| First Author | Johnson KG | Year | 1999 |
| Journal | J Immunol | Volume | 162 |
| Issue | 7 | Pages | 3802-13 |
| PubMed ID | 10201897 | Mgi Jnum | J:53576 |
| Mgi Id | MGI:1332950 | Doi | 10.4049/jimmunol.162.7.3802 |
| Citation | Johnson KG, et al. (1999) TCR signaling thresholds regulating T cell development and activation are dependent upon SHP-1. J Immunol 162(7):3802-13 |
| abstractText | An examination of thymocytes and peripheral T cells from SHP-1-deficient motheaten mice possessing a transgenic MHC class I-restricted TCR has implicated SHP-1 in regulating TCR signaling thresholds at three checkpoints in T cell development and activation. First, in the population of CD4-CD8- double negative thymocytes, SHP-1 appears capable of regulating signals from TCR complexes that control the maturation and proliferation of double negative thymocytes. Second, the loss of SHP-1 increased the number of CD4+CD8+ double positive thymocytes capable of maturing as TCRhigh single positive thymocytes. Third, the loss of SHP-1 altered the basal level of activation of naive lymph node T cells. Accordingly, SHP-1-deficient lymph node T cells bearing the transgenic TCR demonstrated a hyperresponsiveness to stimulation with cognate peptide. However, the loss of SHP-1 did not alter the cytolytic ability of mature effector cytotoxic T lymphocytes. Together these results suggest that SHP-1 contributes to establishing thresholds for TCR signaling in thymocytes and naive peripheral T cells. |
