Evidence map›Paper›PMID 24794441›Full record

ArticleCell reports2014

Interleukin-17D mediates tumor rejection through recruitment of natural killer cells.

Timothy O'Sullivan, Robert Saddawi-Konefka, Emilie Gross, Miller Tran, Stephen P Mayfield, Hiroaki Ikeda, Jack D Bui

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

58 citing papers in PubMed, 84 citations in OpenAlex.

  1. IL-17D reprograms CD93Cellular & molecular immunology · 2026
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  10. The IL-17 family in diseases: from bench to bedside.Signal transduction and targeted therapy · 2023
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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

7 authors at 2 institutions in 2 countries.

Timothy O'SullivanDepartment of Pathology, University of California, San Diego, 9500 Gilman Drive MC 0612, La Jolla, CA 92093, USA.
Robert Saddawi-KonefkaDepartment of Pathology, University of California, San Diego, 9500 Gilman Drive MC 0612, La Jolla, CA 92093, USA.
Emilie GrossDepartment of Pathology, University of California, San Diego, 9500 Gilman Drive MC 0612, La Jolla, CA 92093, USA.
Miller TranDepartment of Biology, University of California, San Diego, 9500 Gilman Drive MC 0612, La Jolla, CA 92093, USA.
Stephen P MayfieldDepartment of Biology, University of California, San Diego, 9500 Gilman Drive MC 0612, La Jolla, CA 92093, USA.
Hiroaki IkedaDepartment of Immuno-Gene Therapy, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Jack D BuiDepartment of Pathology, University of California, San Diego, 9500 Gilman Drive MC 0612, La Jolla, CA 92093, USA. Electronic address: jbui@ucsd.edu.
University of California, San Diego · USMie University · JP

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DIANE M SIMEONE · 1985 to 2026
$124.9M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007198 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHI, NEIL C, INSEL, PAUL A · 1985 to 2024
$29.3M
Innate anti-tumor immune responsesR01CA157885 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BUI, JACK D · 2011 to 2015
$1.8M
The function and regulation of histocompatibility antigen 60 in cancerK08CA128893 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BUI, JACK D · 2008 to 2012
$631k
NCI NIH HHS CA128893NCI NIH HHS CA157885NCI NIH HHS K08 CA128893NCI NIH HHS P30 CA023100NCI NIH HHS R01 CA157885NIGMS NIH HHS T32 GM007198
6 · The paper itself

Abstract

The process of cancer immunoediting generates a repertoire of cancer cells that can persist in immune-competent hosts. In its most complex form, this process begins with the elimination of highly immunogenic unedited tumor cells followed by the escape of less immunogenic edited cells. Although edited tumors can release immunosuppressive factors, it is unknown whether unedited tumors produce cytokines that enhance antitumor function. Utilizing gene microarray analysis, we found the cytokine interleukin 17D (IL-17D) was highly expressed in certain unedited tumors but not in edited mouse tumor cell lines. Moreover, forced expression of IL-17D in edited tumor cells induced rejection by stimulating MCP-1 production from tumor endothelial cells, leading to the recruitment of natural killer (NK) cells. NK cells promoted M1 macrophage development and adaptive immune responses. IL-17D expression was also decreased in certain high-grade and metastatic human tumors, suggesting that it can be targeted for tumor immune therapy.

Indexed as

AnimalsChemokine CCL2HumansInterleukin-17Killer Cells, NaturalMiceMice, Inbred C57BLMice, TransgenicNeoplasmsSarcomaCCL2 protein, humanChemokine CCL2IL17D protein, humanInterleukin-17

Identifiers

PMID24794441
PMCPMC4084720
OpenAlexW2045923059

What OpenQuestion holds

Textmetadata
LicenceTDM
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.