ReviewNature immunology2011
T-bet in disease.
Review in Nature immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
145 citing papers in PubMed.
- Induced expression of FcγRIIIa (CD16a) on CD4+ T cells triggers generation of IFN-γhigh subset.The Journal of biological chemistry · 2015Trial
- CD4 T cells require ICOS-mediated PI3K signaling to increase T-Bet expression in the setting of anti-CTLA-4 therapy.Cancer immunology research · 2014Trial
- Downregulation of T-bet/GATA-3 ratio induced by IL-11 treatment is responsible for Th1/Th2 balance restoration in human immune thrombocytopenic purpura (ITP).Journal of thrombosis and thrombolysis · 2014Trial
- Toxoplasma gondii infection reduces CD59 expression through downregulation of JAK2/STAT3 signaling axis to enhance decidual NK cell cytotoxicity via the RAS/MAPK pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Multicellular crosstalk in neutrophilic asthma: unraveling the pathogenic web of steroid resistance and emerging precision therapies.Journal of translational medicine · 2026Review
- Modulation of the Immune-Inflammatory Microenvironment by Implant Material Properties in Peri-Implantitis.International journal of molecular sciences · 2026Review
- Innate immunity and hypertension: unveiling inflammatory pathways for novel therapies.Frontiers in pharmacology · 2026Review
- Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): diagnosis and management.Journal of translational medicine · 2025Review
- A time-gated PKA-CREB signaling circuit licenses IL-12 responsiveness and Th1 fate in CD4Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- T cells in cancer: mechanistic insights and therapeutic advances.Biomarker research · 2025Review
- Oxymatrine and astragaloside IV co-loaded liposomes: Scale-up purposes and their enhancement of anti-PD-1 efficacy against breast cancer.Materials today. Bio · 2025Article
- STIM1-mediated NFAT signaling synergizes with STAT1 to control T-bet expression and TNature immunology · 2025Article
- Decreased T helper 1 cell function underlies recurrent sinopulmonary infections in the 17q12 deletion syndrome.EBioMedicine · 2025Article
- TBX21 inhibits colorectal cancer metastasis through ARHGAP29/GSK3β inhibitory signaling- and MYCT1/ZO-1 signaling-dependent manner.International journal of biological sciences · 2025Article
- The immune response toFrontiers in microbiology · 2025Review
- Bacterial sepsis causes more dramatic pathogenetic changes in the Th1 pathway than does viral (COVID-19) sepsis: a prospective observational study of whole blood transcriptomes.Virology journal · 2024Observational
- Immunoglobulin class-switch recombination: Mechanism, regulation, and related diseases.MedComm · 2024Review
- Failed Induction of the TIntegrative medicine (Encinitas, Calif.) · 2024Article
- Key Functions of the Transcription Factor BCL6 During T-Cell Differentiation.Advances in experimental medicine and biology · 2024Review
- East meets west: integrating Yin-Yang theory with immunology teaching.Frontiers in immunology · 2024Review
85 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The activation of immune-defense mechanisms in response to a microbial attack must be robust and appropriately tailored to fight particular types of pathogens. Infection with intracellular microorganisms elicits a type 1 inflammatory response characterized by mobilization of T helper type 1 (T(H)1) cells to the site of infection, where they are responsible for the recruitment and activation of macrophages. At the center of the type 1 inflammatory response is the transcription factor T-bet, a critical regulator of the T(H)1 differentiation program. T-bet induces the production of interferon-γ (IFN-γ) and orchestrates the T(H)1 cell-migratory program by regulating the expression of chemokines and chemokine receptors. However, tight regulation of the type 1 inflammatory response is essential for the prevention of immunopathology and the development of organ-specific autoimmunity. In this review, we discuss how T-bet expression drives autoaggressive and inflammatory processes and how its function in vivo must be delicately balanced to avoid disease.
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What OpenQuestion holds
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.