| First Author | Codarri L | Year | 2011 |
| Journal | Nat Immunol | Volume | 12 |
| Issue | 6 | Pages | 560-7 |
| PubMed ID | 21516112 | Mgi Jnum | J:172802 |
| Mgi Id | MGI:5009068 | Doi | 10.1038/ni.2027 |
| Citation | Codarri L, et al. (2011) RORgammat drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation. Nat Immunol 12(6):560-7 |
| abstractText | Although the role of the T(H)1 and T(H)17 subsets of helper T cells as disease mediators in autoimmune neuroinflammation remains a subject of some debate, none of their signature cytokines are essential for disease development. Here we report that interleukin 23 (IL-23) and the transcription factor RORgammat drove expression of the cytokine GM-CSF in helper T cells, whereas IL-12, interferon-gamma (IFN-gamma) and IL-27 acted as negative regulators. Autoreactive helper T cells specifically lacking GM-CSF failed to initiate neuroinflammation despite expression of IL-17A or IFN-gamma, whereas GM-CSF secretion by Ifng(-/-)Il17a(-/-) helper T cells was sufficient to induce experimental autoimmune encephalomyelitis (EAE). During the disease effector phase, GM-CSF sustained neuroinflammation via myeloid cells that infiltrated the central nervous system. Thus, in contrast to all other known helper T cell-derived cytokines, GM-CSF serves a nonredundant function in the initiation of autoimmune inflammation regardless of helper T cell polarization. |
