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

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T-bet controls pathogenicity of CTLs in the heart by separable effects on migration and effector activity.

CD8+ CTL contribute to the pathogenesis of myocarditis and cardiac allograft rejection. Using a transgenic model of myocarditis, we examined the role of the transcription factor T-bet in the differentiation of pathogenic cardiac Ag-specific CTL. We demonstrate that T-bet-deficient CTL are significantly impaired in their ability to cause disease, despite intact proliferation and activation phenotypes. In the absence of T-bet, there is markedly reduced expression of the chemokine receptor CXCR3, and CXCR3-gene knockout CTL are significantly less pathogenic than control CTL. Retroviral-mediated CXCR3 expression in T-bet-deficient CD8+ T cells reconstitutes their ability to infiltrate but not to damage the heart, establishing that CD8+ T cell pathogenicity is related to T-bet-dependent CXCR3 expression, reduced cytotoxicity, and enhanced regulation. These findings highlight the potential therapeutic benefit of targeting T-bet-regulated gene expression and CXCR3-dependent migration in immune-mediated heart disease.[1]

References

  1. T-bet controls pathogenicity of CTLs in the heart by separable effects on migration and effector activity. Taqueti, V.R., Grabie, N., Colvin, R., Pang, H., Jarolim, P., Luster, A.D., Glimcher, L.H., Lichtman, A.H. J. Immunol. (2006) [Pubmed]
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