Evidence map›Paper›PMID 40392614›Full record

ArticleJCI insight2025

IL-1β signaling modulates T follicular helper and regulatory cells in human lymphoid tissues.

Romain Vaineau, Raphaël Jeger-Madiot, Samir Ali-Moussa, Laura Prudhomme, Hippolyte Debarnot, Nicolas Coatnoan, Johanna Dubois, Marie Binvignat, Hélène Vantomme, Bruno Gouritin and 12 more

Abstract read
In one paragraph

Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Review
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  5. Review
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

22 authors.

Romain VaineauImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Raphaël Jeger-MadiotImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Samir Ali-MoussaImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Laura PrudhommeImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Hippolyte DebarnotImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Nicolas CoatnoanImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Johanna DuboisImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Marie BinvignatImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Hélène VantommeImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Bruno GouritinImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Gwladys FourcadeImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Paul EngeroffImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Aude BelbézierImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Romain LuscanDepartment of Pediatric Otolaryngology, AP-HP, Hôpital Necker-Enfants Malades, Paris, France.
Françoise DenoyelleDepartment of Pediatric Otolaryngology, AP-HP, Hôpital Necker-Enfants Malades, Paris, France.
Roberta LorenzonImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Claire RibetImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Michelle RosenzwajgImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Bertrand BellierImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
David KlatzmannImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Nicolas TchitchekImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.
Stéphanie Graff-DuboisImmunology, Immunopathology, Immunotherapy, INSERM U959, Pitié Salpétrière Hospital, Sorbonne University, Paris, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of T follicular helper (Tfh) and T follicular regulatory (Tfr) cell homeostasis in germinal centers (GCs) can lead to antibody-mediated autoimmunity. While IL-1β modulates the GC response via IL-1R1 and IL-1R2 receptors on follicular T cells in animal models, its role in humans remains unclear. We analyzed Tfh and Tfr phenotypes in human secondary lymphoid organs (tonsils, spleen, and mesenteric lymph nodes) using flow cytometry, single-cell transcriptomics, and in vitro culture, comparing findings with samples from autoimmune patients. We observed organ-specific Tfh/Tfr phenotypes according to activation status and IL-1 receptor expression. An excess of IL-1R1 over IL-1R2 expression promoted a unique activated Tfr subset with Treg and GC-Tfh features. IL-1β signaling via IL-1R1 enhanced follicular T cell activation and Tfh-to-Tfr differentiation, while IL-1β inhibition upregulated IL-1R1, indicating a tightly regulated process. In autoimmune patients, high IL-1β and circulating Tfr levels correlated with increased autoantibody production, linking inflammation, IL-1β signaling, and Tfr/Tfh balance. Our findings highlight the critical role of IL-1β in follicular T cell activation and suggest that targeting IL-1β signaling in Tfh and Tfr cells could be a promising strategy for treating antibody-mediated autoimmune diseases.

Indexed as

Interleukin-1betaLymphoid TissueT Follicular Helper CellsT-Lymphocytes, Helper-InducerT-Lymphocytes, RegulatoryAutoimmune DiseasesAutoimmunityCell DifferentiationFemaleGerminal CenterHumansLymphocyte ActivationMaleReceptors, Interleukin-1 Type ISignal TransductionIL1B protein, humanInterleukin-1betaReceptors, Interleukin-1 Type IAutoimmune diseasesAutoimmunityCellular immune responseImmunologyT cells

Identifiers

PMID40392614
PMCPMC12220957

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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.