Evidence map›Paper›PMID 30528455›Full record

ArticleEBioMedicine2019

Concomitant type I IFN and M-CSF signaling reprograms monocyte differentiation and drives pro-tumoral arginase production.

Yuanyuan Tong, Luyang Zhou, Limin Yang, Panpan Guo, Yanlan Cao, F Xiao-Feng Qin, Jianghuai Liu

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

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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 3 institutions in 1 country.

Yuanyuan TongState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Luyang ZhouDepartment of Anesthesiology, Nanjing Gulou Hospital, Affiliated Hospital of Nanjing University Medical School, Nanjing 210008, China.
Limin YangState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Panpan GuoState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Yanlan CaoState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
F Xiao-Feng QinCenter of Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100005, China; Suzhou Institute of Systems Medicine, Suzhou, Jiangsu 215123, China.
Jianghuai LiuState Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing 210061, China. Electronic address: liujianghuai@nju.edu.cn.
Model Animal Research Center · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNNanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType I IFN-based therapies against solid malignancies have yielded only limited success. How IFN affects tumor-associated macrophage (TAM) compartment to impact the therapeutic outcomes are not well understood.

methodsThe effect of an IFN-inducer poly(I:C) on tumor-infiltrating monocytes and TAMs were analyzed using a transplantable mouse tumor model (LLC). In vitro culture systems were utilized to study the direct actions by poly(I:C)-IFN on differentiating monocytes.

resultsWe found that poly(I:C)-induced IFN targets Ly6C

conclusionsTaken together, we have uncovered two functionally opposing actions by IFN on the TAM compartment. Our work provides significant new insights on IFN-mediated immunoregulation that may have implications in cancer therapies.

Indexed as

Signal TransductionAnimalsArginaseCarcinoma, Lewis LungCell DifferentiationCell Line, TumorCellular ReprogrammingInterferon Type IMacrophage Colony-Stimulating FactorMacrophagesMiceMicroRNAsMonocytesNeoplasm TransplantationPoly I-CSTAT3 Transcription FactorArg1 protein, mouseArginaseInterferon Type IMacrophage Colony-Stimulating FactorMicroRNAsMirn155 microRNA, mousePoly I-CStat3 protein, mouseSTAT3 Transcription FactorAnti-tumor immunityArginaseM-CSFMonocyte maturationTumor-associated macrophagesType I IFN

Identifiers

PMID30528455
PMCPMC6354658
OpenAlexW2904252443

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.