| First Author | Yogev N | Year | 2022 |
| Journal | Cell Rep | Volume | 38 |
| Issue | 13 | Pages | 110565 |
| PubMed ID | 35354043 | Mgi Jnum | J:326428 |
| Mgi Id | MGI:7286380 | Doi | 10.1016/j.celrep.2022.110565 |
| Citation | Yogev N, et al. (2022) CD4(+) T-cell-derived IL-10 promotes CNS inflammation in mice by sustaining effector T cell survival. Cell Rep 38(13):110565 |
| abstractText | Interleukin (IL)-10 is considered a prototypical anti-inflammatory cytokine, significantly contributing to the maintenance and reestablishment of immune homeostasis. Accordingly, it has been shown in the intestine that IL-10 produced by Tregs can act on effector T cells, thereby limiting inflammation. Herein, we investigate whether this role also applies to IL-10 produced by T cells during central nervous system (CNS) inflammation. During neuroinflammation, both CNS-resident and -infiltrating cells produce IL-10; yet, as IL-10 has a pleotropic function, the exact contribution of the different cellular sources is not fully understood. We find that T-cell-derived IL-10, but not other relevant IL-10 sources, can promote inflammation in experimental autoimmune encephalomyelitis. Furthermore, in the CNS, T-cell-derived IL-10 acts on effector T cells, promoting their survival and thereby enhancing inflammation and CNS autoimmunity. Our data indicate a pro-inflammatory role of T-cell-derived IL-10 in the CNS. |
