| First Author | Tang C | Year | 2018 |
| Journal | Nat Immunol | Volume | 19 |
| Issue | 7 | Pages | 755-765 |
| PubMed ID | 29915298 | Mgi Jnum | J:305313 |
| Mgi Id | MGI:6706422 | Doi | 10.1038/s41590-018-0134-y |
| Citation | Tang C, et al. (2018) Suppression of IL-17F, but not of IL-17A, provides protection against colitis by inducing Treg cells through modification of the intestinal microbiota. Nat Immunol 19(7):755-765 |
| abstractText | The cytokines IL-17A and IL-17F have 50% amino-acid identity and bind the same receptor; however, their functional differences have remained obscure. Here we found that Il17f(-/-) mice resisted chemically induced colitis, but Il17a(-/-) mice did not, and that Il17f(-/-) CD45RB(hi)CD4(+) T cells induced milder colitis in lymphocyte-deficient Rag2(-/-) mice, accompanied by an increase in intestinal regulatory T cells (Treg cells). Clostridium cluster XIVa in colonic microbiota capable of inducing Treg cells was increased in both Il17f(-/-) mice and mice given transfer Il17f(-/-) T cells, due to decreased expression of a group of antimicrobial proteins. There was substantial production of IL-17F, but not of IL-17A, not only by naive T cells but also by various colon-resident cells under physiological conditions. Furthermore, antibody to IL-17F suppressed the development of colitis, but antibody to IL-17A did not. These observations suggest that IL-17F is an effective target for the treatment of colitis. |
