ArticleBlood2006
T-bet is a critical determinant in the instability of the IL-17-secreting T-helper phenotype.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 144 citations in OpenAlex.
- The transcription factor Twist1 limits T helper 17 and T follicular helper cell development by repressing the gene encoding the interleukin-6 receptor α chain.The Journal of biological chemistry · 2013Trial
- Article
- Factors impacting the benefits and pathogenicity of Th17 cells in the tumor microenvironment.Frontiers in immunology · 2023Review
- GATA3 induces the pathogenicity of Th17 cells via regulating GM-CSF expression.Frontiers in immunology · 2023Article
- Programmed T cell differentiation: Implications for transplantation.Cellular immunology · 2020Review
- The evolving role of T-bet in resistance to infection.Nature reviews. Immunology · 2019Review
- T Helper Cell Differentiation, Heterogeneity, and Plasticity.Cold Spring Harbor perspectives in biology · 2018Review
- Dynamic balance between master transcription factors determines the fates and functions of CD4 T cell and innate lymphoid cell subsets.The Journal of experimental medicine · 2017Review
- STAT3 Activation Impairs the Stability of Th9 Cells.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Mucosal-associated invariant T-cell activation and accumulation after in vivo infection depends on microbial riboflavin synthesis and co-stimulatory signals.Mucosal immunology · 2017Article
- Immune Mechanisms in Arterial Hypertension.Journal of the American Society of Nephrology : JASN · 2016Review
- IL17 Promotes Mammary Tumor Progression by Changing the Behavior of Tumor Cells and Eliciting Tumorigenic Neutrophils Recruitment.Cancer research · 2015Article
- Diverse roles for T-bet in the effector responses required for resistance to infection.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Th17 cells demonstrate stable cytokine production in a proallergic environment.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- The transcription factor Etv5 controls TH17 cell development and allergic airway inflammation.The Journal of allergy and clinical immunology · 2014Article
- T-bet regulates immunity to Francisella tularensis live vaccine strain infection, particularly in lungs.Infection and immunity · 2014Article
- The role of protein modifications of T-bet in cytokine production and differentiation of T helper cells.Journal of immunology research · 2014Review
- Role of cytokines and Toll-like receptors in the immunopathogenesis of Guillain-Barré syndrome.Mediators of inflammation · 2014Review
- Computational modeling of heterogeneity and function of CD4+ T cells.Frontiers in cell and developmental biology · 2014Review
- Faecalibacterium prausnitzii inhibits interleukin-17 to ameliorate colorectal colitis in rats.PloS one · 2014Article
18 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
7 authors at 1 institution in 2 countries.
Funding
Abstract
IL-23, an IL-12-related cytokine, induces an IL-17-secreting T-helper phenotype that is involved in autoimmune diseases and host defense against certain pathogens. Although the transcription factors required for development of IL-23-stimulated cells are unknown, we show that T-bet is a critical negative regulator of the IL-23-primed T-cell phenotype, which we term Th1beta. Th1 or Th1beta Tbx21-/- cultures secrete higher than WT levels of IL-17 in response to T-cell receptor (TCR) or IL-23 + IL-18 stimulation. Ectopic T-bet expression in Th1beta cells promotes IFN-gamma secretion but decreases IL-17 production. Although antigen-receptor stimulation of Th1beta cells stimulates IL-17 production, it also induces the IFN-gamma-independent expression of T-bet and progression to a Th1 cytokine secretion pattern. T-bet is required for the progression to the Th1 phenotype, because Tbx21-/- Th1beta cultures maintain the IL-17-secreting phenotype after 2 weeks of culture. Addition of IFN-gamma to Tbx21-/- Th1beta cultures cannot recover the progression to the Th1 phenotype, suggesting T-bet, rather than IFN-gamma, mediates Th1beta to Th1 progression. The transient nature of the Th1beta phenotype suggests that these cells are a component of type I immunity and that T-bet expression is a critical determinant of Th1 versus Th1beta cell fate.
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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.