| First Author | Veldhoen M | Year | 2006 |
| Journal | Nat Immunol | Volume | 7 |
| Issue | 11 | Pages | 1151-6 |
| PubMed ID | 16998492 | Mgi Jnum | J:113559 |
| Mgi Id | MGI:3686955 | Doi | 10.1038/ni1391 |
| Citation | Veldhoen M, et al. (2006) Signals mediated by transforming growth factor-beta initiate autoimmune encephalomyelitis, but chronic inflammation is needed to sustain disease. Nat Immunol 7(11):1151-6 |
| abstractText | It is unclear whether TGF-beta, a critical differentiation factor for T cells producing interleukin 17 (T(H)-17 cells), is required for the initiation of experimental autoimmune encephalomyelitis (EAE) in vivo. Here we show that mice whose T cells cannot respond to TGF-beta signaling lack T(H)-17 cells and do not develop EAE despite the presence of T helper cell type 1 infiltrates in the spinal cord. Local but not systemic antibody blockade of TGF-beta prevented T(H)-17 cell differentiation and the onset of EAE. The pathogen stimulus zymosan, like mycobacterium, induced T(H)-17 cells and initiated EAE, but the disease was transient and correlated with reduced production of interleukin 23. These data show that TGF-beta is essential for the initiation of EAE and suggest that disease progression may require ongoing chronic inflammation and production of interleukin 23. |
