Evidence map›Paper›PMID 38649353›Full record

ArticleNature communications2024

PD-L1- and IL-4-expressing basophils promote pathogenic accumulation of T follicular helper cells in lupus.

John Tchen, Quentin Simon, Léa Chapart, Morgane K Thaminy, Shamila Vibhushan, Loredana Saveanu, Yasmine Lamri, Fanny Saidoune, Emeline Pacreau, Christophe Pellefigues and 12 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
7.5field-weighted citation impact, top 2% of its field
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

26 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Article
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  8. Article
  9. Basophils in atopic dermatitis: Immunologic roles and clinical implications.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. T follicular helper cells in primary immune regulatory disorders.The Journal of allergy and clinical immunology · 2025
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Chemotherapy-Mediated Induction of PD-L1 via SEI1 Facilitates Myeloma Immune Evasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  20. 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 at 5 institutions in 4 countries.

John Tchen *Université Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.
Quentin Simon *Université Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.ORCID http://orcid.org/0000-0002-2383-2809
Léa ChapartUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.ORCID http://orcid.org/0009-0008-9720-1146
Morgane K ThaminyUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.ORCID http://orcid.org/0009-0002-4842-0277
Shamila VibhushanUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.ORCID http://orcid.org/0000-0001-6196-2295
Loredana SaveanuUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.ORCID http://orcid.org/0000-0003-3138-7968
Yasmine LamriUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.
Fanny SaidouneUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.
Emeline PacreauUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.
Christophe PellefiguesUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.ORCID http://orcid.org/0000-0001-7036-0763
Julie Bex-CoudratUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.
Hajime KarasuyamaInflammation, Infection and Immunity Laboratory, TMDU Advanced Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.ORCID http://orcid.org/0000-0003-0689-0836
Kensuke MiyakeInflammation, Infection and Immunity Laboratory, TMDU Advanced Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.ORCID http://orcid.org/0000-0003-1149-3755
Juan HidalgoUniversidad Autonoma de Barcelona, Facultad de Biociencias, Unidad de Fisiologia Animal Bellaterra, Bellaterra Campus, 08193, Barcelona, Spain.ORCID http://orcid.org/0000-0003-0921-1122
Padraic G FallonSchool of Medicine, Trinity College Dublin, Dublin 2, Ireland.ORCID http://orcid.org/0000-0002-8401-7293
Thomas PapoUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.
Ulrich BlankUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.ORCID http://orcid.org/0000-0002-2661-2983
Marc BenhamouUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.
Guillaume HanounaUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.
Karim SacreUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.ORCID http://orcid.org/0000-0002-6544-234X
Eric DaugasUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France.
Nicolas CharlesUniversité Paris Cité, Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS EMR8252, Faculté de Médecine site Bichat, 75018, Paris, France. nicolas.charles@inserm.fr.ORCID http://orcid.org/0000-0002-5416-5834
Centre National de la Recherche Scientifique · FRUniversité Claude Bernard Lyon 1 · FRTokyo Medical and Dental University · JPTrinity College Dublin · IEUniversitat Autònoma de Barcelona · ES

Funding

Agence Nationale de la Recherche (French National Research Agency) ANR-19-CE17-0029 BALUMETAgence Nationale de la Recherche (French National Research Agency) ANRPIA-10-LABX-0017 INFLAMEXCentre National de la Recherche Scientifique (National Center for Scientific Research) EMR8252Fondation pour la Recherche Médicale (Foundation for Medical Research in France) EQU201903007794Institut National de la Santé et de la Recherche Médicale (National Institute of Health and Medical Research) UMR1149Ministerio de Economía y Competitividad (Ministry of Economy and Competitiveness) RTI2018-101105-B-I00
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by anti-nuclear autoantibodies whose production is promoted by autoreactive T follicular helper (TFH) cells. During SLE pathogenesis, basophils accumulate in secondary lymphoid organs (SLO), amplify autoantibody production and disease progression through mechanisms that remain to be defined. Here, we provide evidence for a direct functional relationship between TFH cells and basophils during lupus pathogenesis, both in humans and mice. PD-L1 upregulation on basophils and IL-4 production are associated with TFH and TFH2 cell expansions and with disease activity. Pathogenic TFH cell accumulation, maintenance, and function in SLO were dependent on PD-L1 and IL-4 in basophils, which induced a transcriptional program allowing TFH2 cell differentiation and function. Our study establishes a direct mechanistic link between basophils and TFH cells in SLE that promotes autoantibody production and lupus nephritis.

Indexed as

B7-H1 AntigenBasophilsInterleukin-4Lupus Erythematosus, SystemicT Follicular Helper CellsAdultAnimalsAutoantibodiesCell DifferentiationFemaleHumansLupus NephritisMaleMiceMice, Inbred C57BLMiddle AgedAutoantibodiesB7-H1 AntigenCD274 protein, humanCd274 protein, mouseIL4 protein, humanIl4 protein, mouseInterleukin-4

Identifiers

PMID38649353
PMCPMC11035650
OpenAlexW4395001516

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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.