| First Author | Park JE | Year | 2018 |
| Journal | Clin Immunol | Volume | 192 |
| Pages | 50-57 | PubMed ID | 29673901 |
| Mgi Jnum | J:360993 | Mgi Id | MGI:7855080 |
| Doi | 10.1016/j.clim.2018.04.007 | Citation | Park JE, et al. (2018) The role of Syk in peripheral T cells. Clin Immunol 192:50-57 |
| abstractText | The aim of this study was to understand how Syk affects peripheral T cell function. T cells from Syk(-/-) chimeric mice and DR1 Syk(fl/fl) CD4(cre) conditional mice gave strong CD3-induced Th1, Th2, and Th17 cytokine responses. However, an altered peptide ligand (APL) of human CII (256-276) with two substitutions (F263N, E266D), also called A12, elicited only Th2 cytokine responses from Syk(fl/fl) T cells but not Syk(fl/fl-)CD4(cre) T cells. Western blots revealed a marked increase in the phosphorylation of Syk, JNK and p38 upon A12/DR1 activation in WT or Syk(fl/fl) T cells but not in Syk(fl/fl)CD4(-cre) cells. We demonstrate that Syk is required for the APL- induction of suppressive cytokines. Chemical Syk inhibitors blocked activation of GATA-3 by peptide A12/DR1. In conclusion, this study provides novel insights into the role that Syk plays in directing T cell activity, and may shape therapeutic approaches for autoimmune diseases. |
