T bet for Th1 response

T
O’Connor RA, Cambrook H, Huettner K, Anderton SM. T-bet is essential for Th1-mediated, but not Th17-mediated, CNS autoimmune disease. Eur J Immunol. 2013 Jul 23. doi: 10.1002/eji.201343689. [Epub ahead of print] 



T cells that produce both IL-17 and IFN-γ, and co-express ROR-γt and T-bet, are often found at sites of autoimmune inflammation. However, it is unknown whether this co-expression of T-bet with ROR-γt is a pre-requisite for immunopathology. We show here that T-bet is not required for the development of Th17-driven experimental autoimmune encephalomyelitis (EAE). The disease was not impaired in T-bet-/- mice and was associated with low IFN-γ production and elevated IL-17 production amongst central nervous system (CNS)-infiltrating CD4+ T cells. T-bet-/- Th17 cells generated in the presence of IL-6/TGF-β/IL-1 and IL-23 produced GM-CSF and high levels of IL-17 and induced disease upon transfer to naïve mice. Unlike their WT counterparts, these T-bet-/- Th17 cells did not exhibit an IL-17→IFN-γ switch upon re-encounter with antigen in the CNS, indicating that this functional change is not critical to disease development. In contrast, T-bet was absolutely required for the pathogenicity of myelin-responsive Th1 cells. T-bet-deficient Th1 cells failed to accumulate in the CNS upon transfer, despite being able to produce GM-CSF. Therefore T-bet is essential for establishing Th1-mediated inflammation but is not required to drive IL-23-induced GM-CSF production, or Th17-mediated autoimmune inflammation
                                           The picture is about gut


T -bet is a signalling molecule in T cells it is involved in T cell response of cells that produce gamma interferon and not the interleukin-17 type of cell thought to be important in autoimmunity

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