Evidence map›Paper›PMID 25667306›Full record

ArticleThe Journal of experimental medicine2015

Immature myeloid cells directly contribute to skin tumor development by recruiting IL-17-producing CD4+ T cells.

Myrna L Ortiz, Vinit Kumar, Anna Martner, Sridevi Mony, Laxminarasimha Donthireddy, Thomas Condamine, John Seykora, Stella C Knight, George Malietzis, Gui Han Lee and 5 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 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.9field-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

55 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. LncRNAInternational journal of biological sciences · 2024
    Article
  6. Article
  7. Review
  8. The IL-17 family in diseases: from bench to bedside.Signal transduction and targeted therapy · 2023
    Review
  9. Article
  10. Review
  11. Review
  12. TInternational journal of molecular sciences · 2022
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
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  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

15 authors at 7 institutions in 3 countries.

Myrna L OrtizH. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612.
Vinit KumarThe Wistar Institute, Philadelphia, PA 19104.
Anna MartnerH. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612 Sahlgrenska Cancer Center, University of Gothenburg, S-405 30 Gothenburg, Sweden.
Sridevi MonyThe Wistar Institute, Philadelphia, PA 19104.
Laxminarasimha DonthireddyThe Wistar Institute, Philadelphia, PA 19104.
Thomas CondamineThe Wistar Institute, Philadelphia, PA 19104.
John SeykoraDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Stella C KnightAntigen Presentation Research Group, Imperial College London, London HA1 3UJ, England, UK.
George MalietzisAntigen Presentation Research Group, Imperial College London, London HA1 3UJ, England, UK St. Mark's Hospital, Harrow HA1 3UJ, England, UK.
Gui Han LeeAntigen Presentation Research Group, Imperial College London, London HA1 3UJ, England, UK St. Mark's Hospital, Harrow HA1 3UJ, England, UK.
Morgan MoorghenSt. Mark's Hospital, Harrow HA1 3UJ, England, UK.
Brianna LenoxH. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612 Sahlgrenska Cancer Center, University of Gothenburg, S-405 30 Gothenburg, Sweden.
Noreen LuettekeH. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612.
Esteban CelisCancer Immunology, Inflammation, and Tolerance Program, Georgia Regents University Cancer Center, Augusta, GA 30912.
Dmitry GabrilovichThe Wistar Institute, Philadelphia, PA 19104 dgabrilovich@wistar.org.
The Wistar Institute · USImperial College London · GBMoffitt Cancer Center · USSt Mark's Hospital · GBUniversity of Gothenburg · SEAugusta University · USUniversity of Pennsylvania · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
Tissue, Pathology and BioinformaticsP50CA168536 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI MULE, JAMES J. · 2013 to 2017
$8.5M
Mechanism of myeloid cell defect in cancerR01CA100062 · NCI · WISTAR INSTITUTE · PI GABRILOVICH, DMITRY I · 2004 to 2018
$4.0M
Understanding molecular mechanisms underlying the formation of the blue nevus andP30AR057217 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI STANLEY, JOHN R · 2009 to 2013
$3.2M
The role of Fyn and Srcasm in UVB-induced cutaneous neoplasiaR01CA165836 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SEYKORA, JOHN T. · 2012 to 2016
$1.6M
Interferon-gamma limits the effectiveness of peptide vaccines for cancerR01CA157303 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI CELIS, ESTEBAN · 2012 to 2017
$1.6M
NCI NIH HHS CA 100062NCI NIH HHS P30 CA010815NCI NIH HHS P50 CA168536NCI NIH HHS R01 CA100062NCI NIH HHS R01 CA157303NCI NIH HHS R01CA157303NCI NIH HHS R01 CA165836NIAMS NIH HHS P30 AR057217
6 · The paper itself

Abstract

Evidence links chronic inflammation with cancer, but cellular mechanisms involved in this process remain unclear. We have demonstrated that in humans, inflammatory conditions that predispose to development of skin and colon tumors are associated with accumulation in tissues of CD33+S100A9+ cells, the phenotype typical for myeloid-derived suppressor cells in cancer or immature myeloid cells (IMCs) in tumor-free hosts. To identify the direct role of these cells in tumor development, we used S100A9 transgenic mice to create the conditions for topical accumulation of these cells in the skin in the absence of infection or tissue damage. These mice demonstrated accumulation of granulocytic IMCs in the skin upon topical application of 12-O-tetradecanoylphorbol-13-acetate (TPA), resulting in a dramatic increase in the formation of papillomas during epidermal carcinogenesis. The effect of IMCs on tumorigenesis was not associated with immune suppression, but with CCL4 (chemokine [C-C motif] ligand 4)-mediated recruitment of IL-17-producing CD4+ T cells. This chemokine was released by activated IMCs. Elimination of CD4+ T cells or blockade of CCL4 or IL-17 abrogated the increase in tumor formation caused by myeloid cells. Thus, this study implicates accumulation of IMCs as an initial step in facilitation of tumor formation, followed by the recruitment of CD4+ T cells.

Indexed as

AnimalsCalgranulin BCD4-Positive T-LymphocytesCell Transformation, NeoplasticChemokine CCL4ColitisFemaleHumansMice, TransgenicMyeloid CellsSkin NeoplasmsTetradecanoylphorbol Acetate12-O-tetradecanoylphorbol-1,3-acetateCalgranulin BChemokine CCL4Tetradecanoylphorbol Acetate

Identifiers

PMID25667306
PMCPMC4354367
OpenAlexW2167188693

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.