| First Author | Harms Pritchard G | Year | 2015 |
| Journal | J Immunol | Volume | 194 |
| Issue | 3 | Pages | 1131-40 |
| PubMed ID | 25556247 | Mgi Jnum | J:337968 |
| Mgi Id | MGI:6843789 | Doi | 10.4049/jimmunol.1401617 |
| Citation | Harms Pritchard G, et al. (2015) Diverse roles for T-bet in the effector responses required for resistance to infection. J Immunol 194(3):1131-40 |
| abstractText | The transcription factor T-bet has been most prominently linked to NK and T cell production of IFN-gamma, a cytokine required for the control of a diverse array of intracellular pathogens. Indeed, in mice challenged with the parasite Toxoplasma gondii, NK and T cell responses are characterized by marked increases of T-bet expression. Unexpectedly, T-bet(-/-) mice infected with T. gondii develop a strong NK cell IFN-gamma response that controls parasite replication at the challenge site, but display high parasite burdens at secondary sites colonized by T. gondii and succumb to infection. The loss of T-bet had a modest effect on T cell production of IFN-gamma but did not impact on the generation of parasite-specific T cells. However, the absence of T-bet resulted in lower T cell expression of CD11a, Ly6C, KLRG-1, and CXCR3 and fewer parasite-specific T cells at secondary sites of infection, associated with a defect in parasite control at these sites. Together, these data highlight T-bet-independent pathways to IFN-gamma production and reveal a novel role for this transcription factor in coordinating the T cell responses necessary to control this infection in peripheral tissues. |
