Evidence map›Paper›PMID 39447575›Full record

ArticleImmunity2024

Transcription factor TCF1 binds to RORγt and orchestrates a regulatory network that determines homeostatic Th17 cell state.

Davide Mangani, Ayshwarya Subramanian, Linglin Huang, Hanning Cheng, S Harsha Krovi, Yufan Wu, Dandan Yang, Thais G Moreira, Giulia Escobar, Alexandra Schnell and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Contextualizing TNature reviews. Immunology · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Davide ManganiGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Institute for Research in Biomedicine, Faculty of Biomedical Sciences, Università della Svizzera Italiana, Bellinzona 6500, Switzerland.
Ayshwarya SubramanianGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Linglin HuangDepartment of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Hanning ChengGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA.
S Harsha KroviGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA.
Yufan WuGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Dandan YangGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA.
Thais G MoreiraGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA.
Giulia EscobarGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA.
Alexandra SchnellGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Karen O DixonGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA.
Rajesh K KrishnanGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA.
Vasundhara SinghBroad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Raymond A SobelDepartment of Pathology, Stanford University, Stanford, CA 94304, USA.
Howard L WeinerGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA.
Vijay K KuchrooGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Ana C AndersonGene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: acanderson@bwh.harvard.edu.

Funding

Role of Negative Costimulation in Regulation of AutoimmunityP01AI039671 · NIAID · YALE UNIVERSITY · PI VIJAY K. KUCHROO · 1996 to 2026
$51.7M
A TCF1:Glucocorticoid regulatory circuit controls IL-23-driven Th17 pathogenicityR01AI176341 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI ANA C ANDERSON · 2023 to 2026
$2.1M
NIAID NIH HHS P01 AI039671NIAID NIH HHS R01 AI176341
6 · The paper itself

Abstract

T helper (Th) 17 cells encompass a spectrum of cell states, including cells that maintain homeostatic tissue functions and pro-inflammatory cells that can drive autoimmune tissue damage. Identifying regulators that determine Th17 cell states can identify ways to control tissue inflammation and restore homeostasis. Here, we found that interleukin (IL)-23, a cytokine critical for inducing pro-inflammatory Th17 cells, decreased transcription factor T cell factor 1 (TCF1) expression. Conditional deletion of TCF1 in mature T cells increased the pro-inflammatory potential of Th17 cells, even in the absence of IL-23 receptor signaling, and conferred pro-inflammatory potential to homeostatic Th17 cells. Conversely, sustained TCF1 expression decreased pro-inflammatory Th17 potential. Mechanistically, TCF1 bound to RORγt, thereby interfering with its pro-inflammatory functions, and orchestrated a regulatory network that determined Th17 cell state. Our findings identify TCF1 as a major determinant of Th17 cell state and provide important insight for the development of therapies for Th17-driven inflammatory diseases.

Indexed as

Hepatocyte Nuclear Factor 1-alphaHomeostasisMice, KnockoutNuclear Receptor Subfamily 1, Group F, Member 3Th17 CellsAnimalsCell DifferentiationGene Expression RegulationInflammationInterleukin-23MiceMice, Inbred C57BLProtein BindingSignal TransductionT Cell Transcription Factor 1Hepatocyte Nuclear Factor 1-alphaHnf1a protein, mouseInterleukin-23Nuclear Receptor Subfamily 1, Group F, Member 3T Cell Transcription Factor 1autoimmunityIL-23multiple sclerosisRORγtTCF1Th17

Identifiers

PMID39447575
PMCPMC11614491

What Socratic holds

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Registered trials

None linked

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 Socratic graph.