| First Author | Sekiya T | Year | 2024 |
| Journal | Cell Rep | Volume | 43 |
| Issue | 3 | Pages | 113954 |
| PubMed ID | 38492221 | Mgi Jnum | J:354842 |
| Mgi Id | MGI:7616017 | Doi | 10.1016/j.celrep.2024.113954 |
| Citation | Sekiya T, et al. (2024) Tonic TCR and IL-1beta signaling mediate phenotypic alterations of naive CD4(+) T cells. Cell Rep 43(3):113954 |
| abstractText | Inert naive CD4(+) T (T(N)) cells differentiate into functional T helper (Th) or regulatory T (Treg) cell subsets upon encountering antigens, mediating properly directed immune responses. Although all T(N) cells can differentiate into any of the Th and Treg cell subsets, heterogeneity exists among T(N) cells. By constructing reporter mice to detect ongoing T cell receptor (TCR) signaling, we identify that interleukin (IL)-1beta signaling affects T(N) cell characteristics, independent of tonic TCR signaling, which also alters T(N) cell phenotypes. IL-1beta reversibly attenuates the differentiation potential of T(N) cells toward Treg cells. IL-1beta signaling is elevated in the splenic T(N) cells, consequently attenuating their differentiation potential toward Treg cells. Aberrant elevation of IL-1beta signaling augments colitogenic activities of T(N) cells. T(N) cells in patients with colitis exhibited elevated IL-1beta signaling. We demonstrate that phenotypic alteration in T(N) cells by IL-1beta is an important mechanism in the regulation of immune responses. |
