ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Diverse roles for T-bet in the effector responses required for resistance to infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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Who cites it
38 citing papers in PubMed, 50 citations in OpenAlex.
- Influence of polyfunctional TbetFrontiers in immunology · 2025Trial
- The cat's out of the bag: Toxoplasma gondii provides further insight into myeloid-mediated host defense.ImmunoHorizons · 2025Review
- A minority of Th1 and Tfh effector cells express survival genes shared by memory cell progeny that require IL-7 or TCR signaling to persist.Cell reports · 2025Article
- Role of Arg1Scientific reports · 2025Article
- Absence of T-box transcription factor 21 limits neuromuscular junction recovery after nerve injury inFrontiers in cell and developmental biology · 2025Article
- The role of KLRG1: a novel biomarker and new therapeutic target.Cell communication and signaling : CCS · 2024Review
- The role of IFN-γ-mediated host immune responses in monitoring and the elimination of Toxoplasma gondii infection.International immunology · 2024Review
- IL-12 Mediates T-bet-Expressing Myeloid Cell-Dependent Host Resistance against Toxoplasma gondii.ImmunoHorizons · 2024Article
- Early T-bet promotes LFA1 upregulation required for CD8+ effector and memory T cell development.The Journal of experimental medicine · 2023Article
- T cell intrinsic STAT1 signaling prevents aberrant Th1 responses during acute toxoplasmosis.Frontiers in immunology · 2023Article
- Immune modulation of Th1/Th2/Treg/Th17/Th9/Th21 cells in rabbits infected withFrontiers in cellular and infection microbiology · 2023Article
- Impact of secondary TCR engagement on the heterogeneity of pathogen-specific CD8+ T cell response during acute and chronic toxoplasmosis.PLoS pathogens · 2022Article
- Th1 cells are dispensable for primary clearance of Chlamydia from the female reproductive tract of mice.PLoS pathogens · 2022Article
- Early Expression of Functional Markers on CD4Frontiers in immunology · 2022Observational
- T-bet-dependent ILC1- and NK cell-derived IFN-γ mediates cDC1-dependent host resistance against Toxoplasma gondii.PLoS pathogens · 2021Article
- Expression Regulation and Function of T-Bet in NK Cells.Frontiers in immunology · 2021Review
- Article
- Novel multiparameter correlates of Coxiella burnetii infection and vaccination identified by longitudinal deep immune profiling.Scientific reports · 2020Article
- Mice Deficient in T-bet Form Inducible NO Synthase-Positive Granulomas That Fail to ConstrainJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Sufficiency of CD40 activation and immune checkpoint blockade for T cell priming and tumor immunity.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
The transcription factor T-bet has been most prominently linked to NK and T cell production of IFN-γ, 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-γ 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-γ 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-γ production and reveal a novel role for this transcription factor in coordinating the T cell responses necessary to control this infection in peripheral tissues.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.