Evidence map›Paper›PMID 36107619›Full record

ArticleJCI insight2022

Keratinocyte-derived cytokine TSLP promotes growth and metastasis of melanoma by regulating the tumor-associated immune microenvironment.

Wenjin Yao, Beatriz German, Dounia Chraa, Antoine Braud, Cecile Hugel, Pierre Meyer, Guillaume Davidson, Patrick Laurette, Gabrielle Mengus, Eric Flatter and 8 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. TSLP: contrasting roles in cancer.Frontiers in immunology · 2025
    Review
  7. Dangerous liaisons: Loss of keratinocyte control over melanocytes in melanomagenesis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Review
  8. Contribution of Keratinocytes in Skin Cancer Initiation and Progression.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Review
  11. Article
  12. 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

18 authors at 3 institutions in 1 country.

Wenjin YaoInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Beatriz GermanInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Dounia ChraaInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Antoine BraudInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Cecile HugelInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Pierre MeyerInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Guillaume DavidsonInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Patrick LauretteInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Gabrielle MengusInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Eric FlatterInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Pierre MarschallInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Justine SegaudInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Marine GuivarchInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Pierre HenerInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Marie-Christine BirlingInstitut Clinique de la Souris (ICS), Illkirch, France.
Dan LipskerDermatology Clinic, Strasbourg University Hospital, Strasbourg, France.
Irwin DavidsonInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Mei LiInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, Inserm U 1258, University of Strasbourg, Illkirch, France.
Centre National de la Recherche Scientifique · FRHôpitaux Universitaires de Strasbourg · FRInstitut Clinique de la Souris · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant melanoma is a major public health issue displaying frequent resistance to targeted therapy and immunotherapy. A major challenge lies in better understanding how melanoma cells evade immune elimination and how tumor growth and metastasis is facilitated by the tumor microenvironment. Here, we show that expression of the cytokine thymic stromal lymphopoietin (TSLP) by epidermal keratinocytes is induced by cutaneous melanoma in both mice and humans. Using genetically engineered models of melanoma and tumor cell grafting combined with TSLP-KO or overexpression, we defined a crosstalk between melanoma cells, keratinocytes, and immune cells in establishing a tumor-promoting microenvironment. Keratinocyte-derived TSLP is induced by signals derived from melanoma cells and subsequently acts via immune cells to promote melanoma progression and metastasis. Furthermore, we show that TSLP signals through TSLP receptor-expressing (TSLPR-expressing) DCs to play an unrecognized role in promoting GATA3+ Tregs expressing a gene signature including ST2, CCR8, ICOS, PD-1, CTLA-4, and OX40 and exhibiting a potent suppressive activity on CD8+ T cell proliferation and IFN-γ production. An analogous population of GATA3-expressing Tregs was also identified in human melanoma tumors. Our study provides insights into the role of TSLP in programming a protumoral immune microenvironment in cutaneous melanoma.

Indexed as

MelanomaSkin NeoplasmsAnimalsCutaneous Malignant MelanomaCytokinesHumansKeratinocytesMiceThymic Stromal LymphopoietinTumor MicroenvironmentCytokinesThymic Stromal LymphopoietinCancer immunotherapyCellular immune responseCytokinesDermatologyOncology

Identifiers

PMID36107619
PMCPMC9675576
OpenAlexW4295909083

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.