Cutting Edge: T-bet and Il-27R Are Critical for In Vivo Ifn- Production by Cd8 T Cells during Infection

Mayer, K.D.; Mohrs, K.; Reiley, W.; Wittmer, S.; Kohlmeier, J.E.; Pearl, J.E.; Cooper, A.M.; Johnson, L.L.; Woodland, D.L.; Mohrs, M.

The Journal of Immunology 180(2): 693-697

2008


DOI: 10.4049/jimmunol.180.2.693
Accession: 068490910

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Abstract
CD8+ T cells are a major source of IFN-gamma, a key effector cytokine in immune responses against many viruses and protozoa. Although the transcription factor T-bet is required for IFN-gamma expression in CD4+ T cells, it is reportedly dispensable in CD8+ T cells, where the transcription factor Eomesodermin is thought to be sufficient. The diverse functions of IFN-gamma are mediated through the IFN-gammaR and STAT1. In CD4+ T cells, STAT1 appears to be critical for the activation of T-bet and IFN-gamma, suggesting an IFN-gamma-dependent positive feedback loop. However, STAT1 can also be activated by other cytokines, including IL-27. In the present study we show that, in contrast to in vitro conditions and the prevailing paradigm, T-bet is critical for the in vivo IFN-gamma production by CD8+ T cells upon infection of mice with diverse pathogens. Whereas IFN-gammaR signals are dispensable for the T-bet-dependent IFN-gamma production, direct IL-27Ralpha signals are critical.