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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Silencing T-bet defines a critical role in the differentiation of autoreactive T lymphocytes.

As a means of developing therapies that target the pathogenic T cells in multiple sclerosis (MS) without compromising the immune system or eliciting systemic side effects, we investigated the use of T-bet-specific antisense oligonucleotides and small interfering RNAs (siRNA) to silence T-bet expression in autoreactive encephalitogenic T cells and evaluated the biological consequences of this suppression in experimental autoimmune encephalomyelitis, a model for MS. The T-bet-specific AS oligonucleotide and siRNA suppressed T-bet expression, IFNgamma production, and STAT1 levels during antigen-specific T cell differentiation. In vitro suppression of T-bet during differentiation of myelin-specific T cells and in vivo administration of a T-bet-specific antisense oligonucleotide or siRNA inhibited disease. T-bet was shown to bind the IFNgamma and STAT1 promoters, but did not regulate the IL-12/STAT4 pathway. Since T-bet regulates IFNgamma production in CD4(+) T cells, but to a lesser extent in most other IFNgamma-producing cells, T-bet may be a target for therapeutics for Th1-mediated diseases.[1]


  1. Silencing T-bet defines a critical role in the differentiation of autoreactive T lymphocytes. Lovett-Racke, A.E., Rocchini, A.E., Choy, J., Northrop, S.C., Hussain, R.Z., Ratts, R.B., Sikder, D., Racke, M.K. Immunity (2004) [Pubmed]
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