Evidence map›Paper›PMID 24769795›Full record

ArticleCellular & molecular immunology2015

Activated cytotoxic lymphocytes promote tumor progression by increasing the ability of 3LL tumor cells to mediate MDSC chemoattraction via Fas signaling.

Fei Yang, Yinxiang Wei, Zhijian Cai, Lei Yu, Lingling Jiang, Chengyan Zhang, Huanmiao Yan, Qingqing Wang, Xuetao Cao, Tingbo Liang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  17. Tumor immunotherapy: New aspects of natural killer cells.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2018
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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

11 authors at 2 institutions in 1 country.

Fei Yang1] Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, China [2] The Second Affiliated Hospital, Hangzhou, Zhejiang, China.
Yinxiang WeiInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Zhijian CaiInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Lei YuInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Lingling JiangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Chengyan ZhangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Huanmiao YanInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Qingqing WangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Xuetao Cao1] Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, China [2] Institute of Immunology and National Key Laboratory of Medical Immunology, Second Military Medical University, Shanghai, China.
Tingbo LiangThe Second Affiliated Hospital, Hangzhou, Zhejiang, China.
Jianli WangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Zhejiang University · CNSecond Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Fas/FasL system transmits intracellular apoptotic signaling, inducing cell apoptosis. However, Fas signaling also exerts non-apoptotic functions in addition to inducing tumor cell apoptosis. For example, Fas signaling induces lung cancer tumor cells to produce prostaglandin E2 (PGE2) and recruit myeloid-derived suppressor cells (MDSCs). Activated cytotoxic T lymphocytes (CTLs) induce and express high levels of FasL, but the effects of Fas activation initiated by FasL in CTLs on apoptosis-resistant tumor cells remain largely unclear. We purified activated CD8(+) T cells from OT-1 mice, evaluated the regulatory effects of Fas activation on tumor cell escape and investigated the relevant mechanisms. We found that CTLs induced tumor cells to secrete PGE2 and increase tumor cell-mediated chemoattraction of MDSCs via Fas signaling, which was favorable to tumor growth. Our results indicate that CTLs may participate in the tumor immune evasion process. To the best of our knowledge, this is a novel mechanism by which CTLs play a role in tumor escape. Our findings implicate a strategy to enhance the antitumor immune response via reduction of negative immune responses to tumors promoted by CTLs through Fas signaling.

Indexed as

Tumor EscapeAnimalsApoptosisCarcinogenesisCell Line, TumorChemotaxisDinoprostoneFas Ligand Proteinfas ReceptorFemaleImmunosuppression TherapyLung NeoplasmsLymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicDinoprostoneFas Ligand Proteinfas ReceptorRNA, Small Interfering

Identifiers

PMID24769795
PMCPMC4654365
OpenAlexW2046288401

What OpenQuestion holds

Textmetadata
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.