ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Tbet or Continued RORγt Expression Is Not Required for Th17-Associated Immunopathology.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- A temporal differentiation program after birth delineates γδ T cell immunity.Science advances · 2026Article
- Metabolic Stress Expands Polyfunctional, Proinflammatory ThArthritis & rheumatology (Hoboken, N.J.) · 2025Article
- The Complex Dysregulations of CD4 T Cell Subtypes in HIV Infection.International journal of molecular sciences · 2024Review
- BHLHE40 Mediates Cross-Talk between Pathogenic TH17 Cells and Myeloid Cells during Experimental Autoimmune Encephalomyelitis.ImmunoHorizons · 2023Article
- Transcriptional and Epigenetic Regulation of Context-Dependent Plasticity in T-Helper Lineages.Immune network · 2023Review
- Transcription factor RORα enforces stability of the Th17 cell effector program by binding to a Rorc cis-regulatory element.Immunity · 2022Article
- Th17 cell plasticity towards a T-bet-dependent Th1 phenotype is required for bacterial control in Staphylococcus aureus infection.PLoS pathogens · 2022Article
- A critical role for Th17 cell-derived TGF-β1 in regulating the stability and pathogenicity of autoimmune Th17 cells.Experimental & molecular medicine · 2021Article
- Th17 Cells in Inflammatory Bowel Disease: Cytokines, Plasticity, and Therapies.Journal of immunology research · 2021Review
- Noncanonical STAT3 activity sustains pathogenic Th17 proliferation and cytokine response to antigen.The Journal of experimental medicine · 2020Article
- Microbiota-Propelled T Helper 17 Cells in Inflammatory Diseases and Cancer.Microbiology and molecular biology reviews : MMBR · 2020Review
- Interplay between Cytokine Circuitry and Transcriptional Regulation Shaping Helper T Cell Pathogenicity and Plasticity in Inflammatory Bowel Disease.International journal of molecular sciences · 2020Review
- IL-23 signaling regulation of pro-inflammatory T-cell migration uncovered by phosphoproteomics.PLoS biology · 2020Article
- Gut Commensal-Induced IκBζ Expression in Dendritic Cells Influences the Th17 Response.Frontiers in immunology · 2020Article
- Cre-loxP Reporter Mouse Reveals Stochastic Activity of theFrontiers in immunology · 2019Article
- mPGES1-Dependent Prostaglandin EJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- Transcriptional signature of human pro-inflammatory TNature communications · 2017Article
- Interleukin 17 is a chief orchestrator of immunity.Nature immunology · 2017Review
- IL-1 signaling is critical for expansion but not generation of autoreactive GM-CSF+ Th17 cells.The EMBO journal · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The discovery of Th17 cell plasticity, in which CD4(+) IL-17-producing Th17 cells give rise to IL-17/IFN-γ double-producing cells and Th1-like IFNγ(+) ex-Th17 lymphocytes, has raised questions regarding which of these cell types contribute to immunopathology during inflammatory diseases. In this study, we show using Helicobacter hepaticus-induced intestinal inflammation that IL-17A(Cre)- or Rag1(Cre)-mediated deletion of Tbx21 has no effect on the generation of IL-17/IFN-γ double-producing cells, but leads to a marked absence of Th1-like IFNγ(+) ex-Th17 cells. Despite the lack of Th1-like ex-Th17 cells, the degree of H. hepaticus-triggered intestinal inflammation in mice in which Tbx21 was excised in IL-17-producing or Rag1-expressing cells is indistinguishable from that observed in control mice. In stark contrast, using experimental autoimmune encephalomyelitis, we show that IL-17A(Cre)-mediated deletion of Tbx21 prevents the conversion of Th17 cells to IL-17A/IFN-γ double-producing cells as well as Th1-like IFN-γ(+) ex-Th17 cells. However, IL-17A(Cre)-mediated deletion of Tbx21 has only limited effects on disease course in this model and is not compensated by Ag-specific Th1 cells. IL-17A(Cre)-mediated deletion of Rorc reveals that RORγt is essential for the maintenance of the Th17 cell lineage, but not immunopathology during experimental autoimmune encephalomyelitis. These results show that neither the single Th17 subset, nor its progeny, is solely responsible for immunopathology or autoimmunity.
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