| First Author | McGinley AM | Year | 2020 |
| Journal | Immunity | Volume | 52 |
| Issue | 2 | Pages | 342-356.e6 |
| PubMed ID | 32023490 | Mgi Jnum | J:288694 |
| Mgi Id | MGI:6431877 | Doi | 10.1016/j.immuni.2020.01.002 |
| Citation | McGinley AM, et al. (2020) Interleukin-17A Serves a Priming Role in Autoimmunity by Recruiting IL-1beta-Producing Myeloid Cells that Promote Pathogenic T Cells. Immunity 52(2):342-356.e6 |
| abstractText | Interleukin-17A (IL-17A) is a major mediator of tissue inflammation in many autoimmune diseases. Anti-IL-17A is an effective treatment for psoriasis and is showing promise in clinical trials in multiple sclerosis. In this study, we find that IL-17A-defective mice or mice treated with anti-IL-17A at induction of experimental autoimmune encephalomyelitis (EAE) are resistant to disease and have defective priming of IL-17-secreting gammadelta T (gammadeltaT17) cells and Th17 cells. However, T cells from Il17a(-/-) mice induce EAE in wild-type mice following in vitro culture with autoantigen, IL-1beta, and IL-23. Furthermore, treatment with IL-1beta or IL-17A at induction of EAE restores disease in Il17a(-/-) mice. Importantly, mobilization of IL-1beta-producing neutrophils and inflammatory monocytes and activation of gammadeltaT17 cells is reduced in Il17a(-/-) mice. Our findings demonstrate that a key function of IL-17A in central nervous system (CNS) autoimmunity is to recruit IL-1beta-secreting myeloid cells that prime pathogenic gammadeltaT17 and Th17 cells. |
