| First Author | Liang D | Year | 2013 |
| Journal | J Immunol | Volume | 191 |
| Issue | 3 | Pages | 1118-25 |
| PubMed ID | 23797670 | Mgi Jnum | J:205731 |
| Mgi Id | MGI:5546302 | Doi | 10.4049/jimmunol.1300626 |
| Citation | Liang D, et al. (2013) IL-23 receptor expression on gammadelta T cells correlates with their enhancing or suppressive effects on autoreactive T cells in experimental autoimmune uveitis. J Immunol 191(3):1118-25 |
| abstractText | We have previously reported that, depending on their activation status, mouse gammadelta T cells can either enhance or inhibit the activity of IL-17(+) autoreactive T cells in experimental autoimmune uveitis. In this study, we showed that gammadelta T cells in naive C57BL/6 (B6) mouse do not express the IL-23R, whereas in immunized mice, it is expressed on >50% of gammadelta T cells. In vitro studies showed that IL-23R expression on gammadelta T cells is modulated by their state of activation, as weakly activated gammadelta T cells expressed the IL-23R, but highly activated gammadelta T cells did not. Functional studies showed that IL-23R(+) gammadelta T cells had the strongest suppressive effect on IL-17(+) autoreactive T cells, and that this effect was inhibited when the IL-23R was blocked by anti-IL-23R Ab or in the presence of excessive amounts of exogenous IL-23. We conclude that the balance between the enhancing and inhibitory effects of gammadelta T cells is regulated by their level of IL-23R expression. The expression of variable IL-23R levels allows gammadelta T cells to have different regulatory effects on adaptive immune responses, conceivably as a result of alphabeta and gammadelta T cells competing for IL-23. |
