| First Author | Wang L | Year | 2024 |
| Journal | Cell Rep | Volume | 43 |
| Issue | 6 | Pages | 114258 |
| PubMed ID | 38781073 | Mgi Jnum | J:351059 |
| Mgi Id | MGI:7665965 | Doi | 10.1016/j.celrep.2024.114258 |
| Citation | Wang L, et al. (2024) T-bet deficiency and Hic1 induction override TGF-beta-dependency in the formation of CD103(+) intestine-resident memory CD8(+) T cells. Cell Rep 43(6):114258 |
| abstractText | Transforming growth factor beta (TGF-beta) represents a well-established signal required for tissue-resident memory T cell (T(RM)) formation at intestinal surfaces, regulating the expression of a large collection of genes coordinately promoting intestinal T(RM) differentiation. The functional contribution from each TGF-beta-controlled transcription factor is not entirely known. Here, we find that TGF-beta-induced T-bet downregulation and Hic1 induction represent two critical events during intestinal T(RM) differentiation. Importantly, T-bet deficiency significantly rescues intestinal T(RM) formation in the absence of the TGF-beta receptor. Hic1 induction further strengthens T(RM) maturation in the absence of TGF-beta and T-bet. Our results reveal that provision of certain TGF-beta-induced molecular events can partially replace TGF-beta signaling to promote the establishment of intestinal T(RM)s, which allows the functional dissection of TGF-beta-induced transcriptional targets and molecular mechanisms for T(RM) differentiation. |