Evidence map›Paper›PMID 25385836›Full record

ArticleThe EMBO journal2014

Chronic exposure to TGFβ1 regulates myeloid cell inflammatory response in an IRF7-dependent manner.

Merav Cohen, Orit Matcovitch, Eyal David, Zohar Barnett-Itzhaki, Hadas Keren-Shaul, Ronnie Blecher-Gonen, Diego Adhemar Jaitin, Antonio Sica, Ido Amit, Michal Schwartz

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

82 citing papers in PubMed, 148 citations in OpenAlex.

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  16. Key immune regulators in retinal ischemia-reperfusion injuryInternational journal of ophthalmology · 2025
    Article
  17. Article
  18. Review
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22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Merav CohenDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Orit MatcovitchDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, Israel Department of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Eyal DavidDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Zohar Barnett-ItzhakiDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Hadas Keren-ShaulDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Ronnie Blecher-GonenDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Diego Adhemar JaitinDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Antonio SicaHumanitas Clinical and Research Center, Rozzano Milan, Italy DiSCAFF, University of Piemonte Orientale A. Avogadro, Novara, Italy.
Ido AmitDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel ido.amit@weizmann.ac.il michal.schwartz@weizmann.ac.il.
Michal SchwartzDepartment of Neurobiology, Weizmann Institute of Science, Rehovot, Israel ido.amit@weizmann.ac.il michal.schwartz@weizmann.ac.il.
Weizmann Institute of Science · ILHumanitas University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tissue microenvironment influences the function of resident and infiltrating myeloid-derived cells. In the central nervous system (CNS), resident microglia and freshly recruited infiltrating monocyte-derived macrophages (mo-MΦ) display distinct activities under pathological conditions, yet little is known about the microenvironment-derived molecular mechanism that regulates these differences. Here, we demonstrate that long exposure to transforming growth factor-β1 (TGFβ1) impaired the ability of myeloid cells to acquire a resolving anti-inflammatory phenotype. Using genome-wide expression analysis and chromatin immunoprecipitation followed by next-generation sequencing, we show that the capacity to undergo pro- to anti-inflammatory (M1-to-M2) phenotype switch is controlled by the transcription factor interferon regulatory factor 7 (IRF7) that is down-regulated by the TGFβ1 pathway. RNAi-mediated perturbation of Irf7 inhibited the M1-to-M2 switch, while IFNβ1 (an IRF7 pathway activator) restored it. In vivo induction of Irf7 expression in microglia, following spinal cord injury, reduced their pro-inflammatory activity. These results highlight the key role of tissue-specific environmental factors in determining the fate of resident myeloid-derived cells under both physiological and pathological conditions.

Indexed as

AnimalsChromatin ImmunoprecipitationGene Expression ProfilingGene Expression RegulationHigh-Throughput Nucleotide SequencingInterferon Regulatory Factor-7Mice, Inbred C57BLMyeloid CellsTransforming Growth Factor beta1Interferon Regulatory Factor-7Irf7 protein, mouseTransforming Growth Factor beta1central nervous systemIRF7myeloid cellsphenotype‐switchTGFβ

Identifiers

PMID25385836
PMCPMC4282639
OpenAlexW2096225770

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.