Evidence map›Paper›PMID 30323677›Full record

ArticleCancer management and research2018

IL-17 induces macrophages to M2-like phenotype via NF-κB.

Jing Shen, Xin Sun, Bo Pan, Shoubo Cao, Jingyan Cao, Dehai Che, Fang Liu, Shuai Zhang, Yan Yu

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

45 citing papers in PubMed, 68 citations in OpenAlex.

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  18. Production of a p65Innate immunity · 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

9 authors at 1 institution in 1 country.

Jing ShenDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, People's Republic of China, yuyan@ems.hrbmu.edu.cn.
Xin SunDepartment of Cardiology, The First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, People's Republic of China.
Bo PanDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, People's Republic of China, yuyan@ems.hrbmu.edu.cn.
Shoubo CaoDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, People's Republic of China, yuyan@ems.hrbmu.edu.cn.
Jingyan CaoDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, People's Republic of China, yuyan@ems.hrbmu.edu.cn.
Dehai CheDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, People's Republic of China, yuyan@ems.hrbmu.edu.cn.
Fang LiuDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, People's Republic of China, yuyan@ems.hrbmu.edu.cn.
Shuai ZhangDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, People's Republic of China, yuyan@ems.hrbmu.edu.cn.
Yan YuDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, People's Republic of China, yuyan@ems.hrbmu.edu.cn.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor-associated macrophage (TAM) is emerging as one of the important complications in cancer promotion. Interleukin-17 (IL-17), a potent pro-inflammatory cytokine, plays an active role in promoting M2 macrophage differentiation (TAMs are M2-like phenotypes). In this study, we aimed to evaluate that IL-17 stimulates key phenotypic and functional signatures of M2 macrophages associated with cancer progression in non-small-cell lung cancer (NSCLC) patients. PATIENTS AND

methodsThe markers and cytokines of M2 macrophages were detected in THP-1-derived macrophages and mouse peritoneal macrophages treated with IL-17. The activation of nuclear factor kappa B (NF-κB) and nuclear localization of p65 in IL-17-treated cells were investigated. The BAY11-7082 inhibitor and the siRNA of p65 were used to block the NF-κB activation. A total of 85 patients who underwent surgery for histologically verified NSCLC were enrolled in this study. The expression of IL-17 and M2 macrophage markers were assessed by immunostaining. Survivals were estimated using the Kaplan-Meier method.

resultsThe CD163 and CD206 cell surface markers and transforming growth factor beta (TGF-β), vascular endothelial growth factor (VEGF) and IL-10 of M2 macrophages were significantly increased in IL-17-treated THP-1-derived macrophages in a dose-dependent manner. IL-17 increased the mRNA levels of Arginase I and Fizz1, the phosphorylation of IkBα and nuclear localization of p65 (a subunit of NF-κB). The BAY11-7082 abrogated IL-17-induced CD206 and CD163 expression, TGF-β, VEGF, IL-10, Arginase I and Fizz1 expression and p65 nuclear translocation. Further experiments showed that IL-17 induced the expression of CD206, CD163, Arginase I, Fizz1 and Ym1 in mouse peritoneal macrophages that were inhibited by siRNA of p65. The immunostaining experiments on human NSCLC tissues indicated that high IL-17 expression was significantly correlated with CD163 and c-Maf. The intratumoral IL-17+ CD163+ c-Maf+ cells were associated with NSCLC progression.

conclusionIL-17 stimulated macrophages to M2-like phenotypes via NF-κB activation. IL-17 may be a potential therapeutic target for NSCLC.

Indexed as

IL-17M2 macrophagesNF-κBnon-small-cell lung cancersurvival

Identifiers

PMID30323677
PMCPMC6177522
OpenAlexW2895665988

What OpenQuestion holds

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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.