| First Author | Muñoz M | Year | 2021 |
| Journal | Proc Natl Acad Sci U S A | Volume | 118 |
| Issue | 6 | PubMed ID | 33526653 |
| Mgi Jnum | J:304411 | Mgi Id | MGI:6507117 |
| Doi | 10.1073/pnas.2002787118 | Citation | Munoz M, et al. (2021) Th2 cells lacking T-bet suppress naive and memory T cell responses via IL-10. Proc Natl Acad Sci U S A 118(6):e2002787118 |
| abstractText | Exacerbated immune responses and loss of self-tolerance lead to the development of autoimmunity and immunopathology. Novel therapies to target autoreactive T cells are still needed. Here, we report that Th2-polarized T cells lacking the transcription factor T-bet harbor strong immunomodulatory potential and suppress antigen-specific CD8(+) T cells via IL-10. Tbx21 (-/-) Th2 cells protected mice against virus-induced type 1 diabetes development and suppressed not only naive but also memory CD8(+) T cell responses. IL-10-producing, but not IL-10-deficient Tbx21 (-/-) Th2 cells down-regulated costimulatory molecules on dendritic cells and reduced their IL-12 production after lymphocytic choriomeningitis virus infection. Impaired dendritic cell activation hindered effector and cytotoxic CD8(+) T cell development after infection. These findings indicate that Tbx21 (-/-) Th2 cells strongly suppress proinflammatory responses of naive and memory T cells via IL-10. Thus, in vivo IL-10-secreting Th2 cells could harbor a therapeutic potential for the treatment of T cell-mediated inflammatory disorders. |
