| First Author | Niedbala W | Year | 2013 |
| Journal | J Immunol | Volume | 191 |
| Issue | 1 | Pages | 164-70 |
| PubMed ID | 23720815 | Mgi Jnum | J:205367 |
| Mgi Id | MGI:5544686 | Doi | 10.4049/jimmunol.1202580 |
| Citation | Niedbala W, et al. (2013) Nitric oxide-induced regulatory T cells inhibit Th17 but not Th1 cell differentiation and function. J Immunol 191(1):164-70 |
| abstractText | NO is a free radical with pleiotropic functions. We have shown earlier that NO induces a population of CD4(+)CD25(+)Foxp3(-) regulatory T cells (NO-Tregs) that suppress the functions of CD4(+)CD25(-) effector T cells in vitro and in vivo. We report in this study an unexpected finding that NO-Tregs suppressed Th17 but not Th1 cell differentiation and function. In contrast, natural Tregs (nTregs), which suppressed Th1 cells, failed to suppress Th17 cells. Consistent with this observation, NO-Tregs inhibited the expression of retinoic acid-related orphan receptor gammat but not T-bet, whereas nTregs suppressed T-bet but not retinoic acid-related orphan receptor gammat expression. The NO-Treg-mediated suppression of Th17 was partially cell contact-dependent and was associated with IL-10. In vivo, adoptively transferred NO-Tregs potently attenuated experimental autoimmune encephalomyelitis. The disease suppression was accompanied by a reduction of Th17, but not Th1 cells in the draining lymph nodes, and a decrease in the production of IL-17, but an increase in IL-10 synthesis. Our results therefore demonstrate the differential suppressive function between NO-Tregs and nTregs and indicate specialization of the regulatory mechanism of the immune system. |
