| First Author | Oh SJ | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 12 | Pages | 6815-21 |
| PubMed ID | 21572032 | Mgi Jnum | J:175480 |
| Mgi Id | MGI:5285789 | Doi | 10.4049/jimmunol.1003916 |
| Citation | Oh SJ, et al. (2011) Invariant NKT cells producing IL-4 or IL-10, but not IFN-gamma, inhibit the Th1 response in experimental autoimmune encephalomyelitis, whereas none of these cells inhibits the Th17 response. J Immunol 186(12):6815-21 |
| abstractText | Experimental autoimmune encephalomyelitis (EAE) is mediated by Th1 and Th17 cells. Invariant NKT (iNKT) cells prevent EAE in an IL-4-, IL-10-, and IFN-gamma-dependent manner. However, which of the iNKT cell-produced cytokines regulates the Th1 or Th17 response in EAE remains unclear. Wild-type B6 and Jalpha18(-/-) mice were immunized with MOG(35-55) peptide to address this issue. Clinical scores for EAE, IL-17, and IFN-gamma transcript levels, and IL-17- or IFN-gamma-expressing CD4(+) T cell percentages in the CNS and draining lymph nodes were higher in Jalpha18(-/-) than in B6 mice, but all of these parameters in the CNS were reduced by the adoptive transfer of wild-type or IFN-gamma-deficient iNKT cells into the Jalpha18(-/-) mice before immunization. In contrast, adoptive transfer of IL-4- or IL-10-deficient iNKT cells into Jalpha18(-/-) mice decreased IL-17 transcript levels and the percentage of IL-17-expressing CD4(+) T cells in the CNS but did not affect clinical scores, IFN-gamma transcript levels, or the percentage of IFN-gamma-expressing CD4(+) T cells in the CNS. Taken together, IL-4- and IL-10-producing iNKT cells inhibit the Th1 cell response, but not the Th17 cell response, although wild-type iNKT cells suppress both the Th1 and Th17 responses in the CNS during EAE. Moreover, IFN-gamma-producing iNKT cells have a minimal role in the regulation of the Th1 and Th17 responses in EAE. |
