| First Author | K?hne M | Year | 2025 |
| Journal | Cell Rep | Volume | 44 |
| Issue | 7 | Pages | 115866 |
| PubMed ID | 40531625 | Mgi Jnum | J:370027 |
| Mgi Id | MGI:8220603 | Doi | 10.1016/j.celrep.2025.115866 |
| Citation | Kohne M, et al. (2025) Satb1 directs the differentiation of T(H)17 cells through suppression of IL-2 expression. Cell Rep 44(7):115866 |
| abstractText | T helper (T(H))17 cells are crucial for host defense in barrier organs, and their altered functionality can disrupt tissue homeostasis, increasing the risk of autoimmune diseases. Thus, it is essential to understand the mechanisms controlling T(H)17 differentiation to develop strategies influencing their role in diseases. Here, we identified Special AT-rich sequence-binding protein 1 (Satb1) as a pioneering factor for T(H)17 development. Satb1 is highly expressed in T(H)17 cells, and loss of Satb1 prevents the differentiation of T(H)17 cells. Consequently, expression of Satb1 in CD4(+) T cells is required for the formation of T(H)17-driven autoimmune diseases. Mechanistically, Satb1 mediates T(H)17 development through regulating accessibility of the Il2 gene locus and thereby preventing interleukin (IL)-2 signaling early during T(H)17 differentiation. Hence, suppression of IL-2 expression by Satb1 during T(H)17 formation is pivotal, suggesting that Satb1 could serve as a novel therapeutic target for treating autoimmune diseases driven by T(H)17 cells. |
