Evidence map›Paper›PMID 40195474›Full record

ArticleCellular & molecular immunology2025

The intrinsic expression of NLRP3 in Th17 cells promotes their protumor activity and conversion into Tregs.

Théo Accogli, Christophe Hibos, Lylou Milian, Mannon Geindreau, Corentin Richard, Etienne Humblin, Romain Mary, Sandy Chevrier, Elise Jacquin, Antoine Bernard and 8 more

Abstract read
In one paragraph

Article in Cellular & molecular immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Review
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  3. T cell-intrinsic PRR signaling in immunity and pathology.Acta biochimica et biophysica Sinica · 2026
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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

18 authors.

Théo AccogliINSERM, Dijon, France.
Christophe Hibos *University of Burgundy, Dijon, France.ORCID 0000-0003-0191-363X
Lylou Milian *INSERM, Dijon, France.
Mannon GeindreauINSERM, Dijon, France.
Corentin RichardUnité de Biologie Moléculaire-Department of Biology and Pathology of Tumors, Georges-Francois Leclerc Cancer Center-UNICANCER, Dijon, France.
Etienne HumblinUniversity of Burgundy, Dijon, France.
Romain MaryUniversity of Burgundy, Dijon, France.
Sandy ChevrierUnité de Biologie Moléculaire-Department of Biology and Pathology of Tumors, Georges-Francois Leclerc Cancer Center-UNICANCER, Dijon, France.
Elise JacquinINSERM, Dijon, France.ORCID 0000-0003-0368-4113
Antoine BernardUniversity of Burgundy, Dijon, France.
Fanny ChalminCancer Biology Transfer Platform, Georges-Francois Leclerc Cancer Center-UNICANCER, Dijon, France.
Catherine PaulLIIC, EA7269, Université de Bourgogne Franche Comté, Dijon, France.
Berhard RyffelLaboratory of Experimental and Molecular Immunology and Neurogenetics (INEM), UMR 7355 CNRS-University of Orleans, Orléans, France.ORCID 0000-0003-2897-8230
Lionel ApetohBrown Center for Immunotherapy, Indiana University Melvin and Bren Simon Comprehensive Cancer Center, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0002-2774-438X
Romain BoidotUnité de Biologie Moléculaire-Department of Biology and Pathology of Tumors, Georges-Francois Leclerc Cancer Center-UNICANCER, Dijon, France.
Mélanie BruchardINSERM, Dijon, France.
François GhiringhelliINSERM, Dijon, France.ORCID 0000-0002-5465-8305
Frédérique VegranINSERM, Dijon, France. frederique.vegran@inserm.fr.ORCID 0000-0002-4377-1441

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Th17 cells can perform either regulatory or inflammatory functions depending on the cytokine microenvironment. These plastic cells can transdifferentiate into Tregs during inflammation resolution, in allogenic heart transplantation models, or in cancer through mechanisms that remain poorly understood. Here, we demonstrated that NLRP3 expression in Th17 cells is essential for maintaining their immunosuppressive functions through an inflammasome-independent mechanism. In the absence of NLRP3, Th17 cells produce more inflammatory cytokines (IFNγ, Granzyme B, TNFα) and exhibit reduced immunosuppressive activity toward CD8+ cells. Moreover, the capacity of NLRP3-deficient Th17 cells to transdifferentiate into Treg-like cells is lost. Mechanistically, NLRP3 in Th17 cells interacts with the TGF-β receptor, enabling SMAD3 phosphorylation and thereby facilitating the acquisition of immunosuppressive functions. Consequently, the absence of NLRP3 expression in Th17 cells from tumor-bearing mice enhances CD8 + T-cell effectiveness, ultimately inhibiting tumor growth.

Indexed as

NLR Family, Pyrin Domain-Containing 3 ProteinTh17 CellsT-Lymphocytes, RegulatoryAnimalsCD8-Positive T-LymphocytesCell DifferentiationCytokinesInflammasomesMiceMice, Inbred C57BLMice, KnockoutSmad3 ProteinCytokinesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseSmad3 ProteinCancer ImmunologyNLRP3Th17 cellsTregsTumor microenvironment

Identifiers

PMID40195474
PMCPMC12041534

What OpenQuestion holds

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Registered trials

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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.