Journal
JOURNAL OF IMMUNOLOGY
Volume 194, Issue 3, Pages 1131-1140Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1401617
Keywords
-
Categories
Funding
- National Institutes of Health [AI-42334, 2T32AI007532-16]
- Commonwealth of Pennsylvania
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available