Evidence map›Paper›PMID 25584012›Full record

ArticleThe Journal of experimental medicine2015

Bee venom processes human skin lipids for presentation by CD1a.

Elvire A Bourgeois, Sumithra Subramaniam, Tan-Yun Cheng, Annemieke De Jong, Emilie Layre, Dalam Ly, Maryam Salimi, Annaliza Legaspi, Robert L Modlin, Mariolina Salio and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
16.6field-weighted citation impact, top 1% 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

69 citing papers in PubMed, 102 citations in OpenAlex.

  1. CD1a and Lipids as Mediators of T Cell Activation in the Skin.The Journal of investigative dermatology · 2025
    Review
  2. CD1a and skin T cells: a pathway for therapeutic intervention.Clinical and experimental dermatology · 2024
    Review
  3. The Immunology of Psoriasis-Current Concepts in Pathogenesis.Clinical reviews in allergy & immunology · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. CD1 displays its own negative regulators.Current opinion in immunology · 2023
    Review
  9. Group AScience immunology · 2023
    Article
  10. Article
  11. Article
  12. Atopic Dermatitis: The Fate of the Fat.International journal of molecular sciences · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Novel Molecular Insights into Human Lipid-Mediated T Cell Immunity.International journal of molecular sciences · 2021
    Review
  20. CD1a function in human skin disease.Molecular immunology · 2021
    Review

9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 3 countries.

Elvire A BourgeoisDivision of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, 02114.
Sumithra SubramaniamMRC Human Immunology Unit, Weatherall Institute of Molecular Medicine and University of Oxford NIHR Biomedical Research Centre, Oxford, Oxfordshire OX3 9DS, England, UK MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine and University of Oxford NIHR Biomedical Research Centre, Oxford, Oxfordshire OX3 9DS, England, UK.
Tan-Yun ChengDivision of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, 02114.
Annemieke De JongDivision of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, 02114.
Emilie LayreDivision of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, 02114.
Dalam LyDivision of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, 02114.
Maryam SalimiMRC Human Immunology Unit, Weatherall Institute of Molecular Medicine and University of Oxford NIHR Biomedical Research Centre, Oxford, Oxfordshire OX3 9DS, England, UK MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine and University of Oxford NIHR Biomedical Research Centre, Oxford, Oxfordshire OX3 9DS, England, UK.
Annaliza LegaspiDivision of Dermatology, David Geffen School of Medicine, Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, CA 90095 Division of Dermatology, David Geffen School of Medicine, Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, CA 90095.
Robert L ModlinDivision of Dermatology, David Geffen School of Medicine, Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, CA 90095 Division of Dermatology, David Geffen School of Medicine, Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, CA 90095.
Mariolina SalioMRC Human Immunology Unit, Weatherall Institute of Molecular Medicine and University of Oxford NIHR Biomedical Research Centre, Oxford, Oxfordshire OX3 9DS, England, UK MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine and University of Oxford NIHR Biomedical Research Centre, Oxford, Oxfordshire OX3 9DS, England, UK.
Vincenzo CerundoloMRC Human Immunology Unit, Weatherall Institute of Molecular Medicine and University of Oxford NIHR Biomedical Research Centre, Oxford, Oxfordshire OX3 9DS, England, UK MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine and University of Oxford NIHR Biomedical Research Centre, Oxford, Oxfordshire OX3 9DS, England, UK.
D Branch MoodyDivision of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, 02114 bmoody@partners.org graham.ogg@ndm.ox.ac.uk.
Graham OggMRC Human Immunology Unit, Weatherall Institute of Molecular Medicine and University of Oxford NIHR Biomedical Research Centre, Oxford, Oxfordshire OX3 9DS, England, UK MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine and University of Oxford NIHR Biomedical Research Centre, Oxford, Oxfordshire OX3 9DS, England, UK bmoody@partners.org graham.ogg@ndm.ox.ac.uk.
Brigham and Women's Hospital · USInstitute of Molecular Medicine · INUniversity of California, Los Angeles · USUniversity of Oxford · GB

Funding

TCR GAMMA/DELTA LYMPHOCYTES IN HUMAN SKIN LESIONSR01AR040312 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MODLIN, ROBERT L · 1990 to 2025
$10.4M
CD1 Presentation of Self Lipids to Human T CellsR01AR048632 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI MOODY, DAVID BRANCH · 2002 to 2024
$9.4M
CD1 autoreactive T cells in human inflammatory skin diseaseR37AR048632 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI DAVID Branch MOODY · 2025 to 2026
$1.1M
Cancer Research UK 11331Cancer Research UK 17722Cancer Research UK C399/A2291Medical Research Council G1000800Medical Research Council MC_UU_12010/1Medical Research Council MC_UU_12010/5NIAMS NIH HHS R01 AR040312NIAMS NIH HHS R37 AR048632
6 · The paper itself

Abstract

Venoms frequently co-opt host immune responses, so study of their mode of action can provide insight into novel inflammatory pathways. Using bee and wasp venom responses as a model system, we investigated whether venoms contain CD1-presented antigens. Here, we show that venoms activate human T cells via CD1a proteins. Whereas CD1 proteins typically present lipids, chromatographic separation of venoms unexpectedly showed that stimulatory factors partition into protein-containing fractions. This finding was explained by demonstrating that bee venom-derived phospholipase A2 (PLA2) activates T cells through generation of small neoantigens, such as free fatty acids and lysophospholipids, from common phosphodiacylglycerides. Patient studies showed that injected PLA2 generates lysophospholipids within human skin in vivo, and polyclonal T cell responses are dependent on CD1a protein and PLA2. These findings support a previously unknown skin immune response based on T cell recognition of CD1a proteins and lipid neoantigen generated in vivo by phospholipases. The findings have implications for skin barrier sensing by T cells and mechanisms underlying phospholipase-dependent inflammatory skin disease.

Indexed as

AnimalsAntigen PresentationAntigens, CD1Bee VenomsCell LineFatty AcidsHumansLigandsLipidsLymphocyte ActivationLysophospholipidsPhospholipases A2SkinT-Cell Antigen Receptor SpecificityT-Lymphocyte SubsetsAntigens, CD1Bee VenomsCD1a antigenFatty AcidsLigandsLipidsLysophospholipidsPhospholipases A2

Identifiers

PMID25584012
PMCPMC4322046
OpenAlexW2139048210

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

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 OpenQuestion graph.