It is unclear whether TGF-, a critical differentiation factor for T cells producing interleukin 17 (TH-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- signaling lack TH-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- prevented TH-17 cell differentiation and the onset of EAE. The pathogen stimulus zymosan, like mycobacterium, induced TH-17 cells and initiated EAE, but the disease was transient and correlated with reduced production of interleukin 23. These data show that TGF- is essential for the initiation of EAE and suggest that disease progression may require ongoing chronic inflammation and production of interleukin 23.
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initiate autoimmune encephalomyelitis, but chronic inflammation is needed to sustain disease
, a critical differentiation factor for T cells producing interleukin 17 (TH-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-
