Your browser version may not work well with NCBI's Web applications. More information here...
Related Articles, Links
Click here to read Click here to read
Cutting edge: T-bet and IL-27R are critical for in vivo IFN-gamma production by CD8 T cells during infection.

Mayer KD, Mohrs K, Reiley W, Wittmer S, Kohlmeier JE, Pearl JE, Cooper AM, Johnson LL, Woodland DL, Mohrs M.

Trudeau Institute, Saranac Lake, NY 12983, USA.

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.

Publication Types:
PMID: 18178806 [PubMed - indexed for MEDLINE]