| First Author | Cunningham CA | Year | 2016 |
| Journal | J Immunol | Volume | 196 |
| Issue | 10 | Pages | 4003-13 |
| PubMed ID | 27084103 | Mgi Jnum | J:261832 |
| Mgi Id | MGI:6158776 | Doi | 10.4049/jimmunol.1501728 |
| Citation | Cunningham CA, et al. (2016) POSH Regulates CD4+ T Cell Differentiation and Survival. J Immunol 196(10):4003-13 |
| abstractText | The scaffold molecule POSH is crucial for the regulation of proliferation and effector function in CD8(+) T cells. However, its role in CD4(+) T cells is not known. In this study, we found that disruption of the POSH scaffold complex established a transcriptional profile that strongly skewed differentiation toward Th2, led to decreased survival, and had no effect on cell cycle entry. This is in stark contrast to CD8(+) T cells in which POSH regulates cell cycle and does not affect survival. Disruption of POSH in CD4(+) T cells resulted in the loss of Tak1-dependent activation of JNK1/2 and Tak1-mediated survival. However, in CD8(+) T cells, POSH regulates only JNK1. Remarkably, each type of T cell had a unique composition of the POSH scaffold complex and distinct posttranslational modifications of POSH. These data indicate that the mechanism that regulates POSH function in CD4(+) T cells is different from CD8(+) T cells. All together, these data strongly suggest that POSH is essential for the integration of cell-type-specific signals that regulate the differentiation, survival, and function of T cells. |
