Evidence map›Paper›PMID 26874522›Full record

ArticleProtein & cell2016

RBP-J is required for M2 macrophage polarization in response to chitin and mediates expression of a subset of M2 genes.

Julia Foldi, Yingli Shang, Baohong Zhao, Lionel B Ivashkiv, Xiaoyu Hu

Abstract read
In one paragraph

Article in Protein & cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–field-weighted citation impact
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

32 citing papers in PubMed.

  1. Review
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  7. Review
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  14. Notch signaling pathway: architecture, disease, and therapeutics.Signal transduction and targeted therapy · 2022
    Review
  15. Article
  16. Saudi journal of biological sciences · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Regulatory network mediated by RBP-J/NFATc1-miR182 controls inflammatory bone resorption.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
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

5 authors.

Julia FoldiGraduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Graduate School of Medical Sciences, New York, NY, 10021, USA.
Yingli ShangSchool of Medicine and Institute for Immunology, Tsinghua University, Beijing, 100084, China.
Baohong ZhaoArthritis and Tissue Degeneration Program, Hospital for Special Surgery, New York, NY, 10021, USA.
Lionel B IvashkivGraduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Graduate School of Medical Sciences, New York, NY, 10021, USA. ivashkivl@hss.edu.
Xiaoyu HuSchool of Medicine and Institute for Immunology, Tsinghua University, Beijing, 100084, China. xiaoyuhu@tsinghua.edu.cn.

Funding

Inhibition of STAT3 and inflammatory cytokine productionR01AI044938 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 2000 to 2025
$9.2M
Fc Receptors &Cytokine Balance in Rheumatoid ArthritisR01AR050401 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI Lionel B Ivashkiv · 2004 to 2026
$7.4M
Regulation of Osteoclastogenesis and Arthritic Bone Resorption by RBP-JR00AR062047 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI ZHAO, BAOHONG · 2014 to 2016
$747k
NIAID NIH HHS R01 AI044938NIAMS NIH HHS R00 AR062047NIAMS NIH HHS R01 AR050401
6 · The paper itself

Abstract

Development of alternatively activated (M2) macrophage phenotypes is a complex process that is coordinately regulated by a plethora of pathways and factors. Here, we report that RBP-J, a DNA-binding protein that integrates signals from multiple pathways including the Notch pathway, is critically involved in polarization of M2 macrophages. Mice deficient in RBP-J in the myeloid compartment exhibited impaired M2 phenotypes in vivo in a chitin-induced model of M2 polarization. Consistent with the in vivo findings, M2 polarization was partially compromised in vitro in Rbpj-deficient macrophages as demonstrated by reduced expression of a subset of M2 effector molecules including arginase 1. Functionally, myeloid Rbpj deficiency impaired M2 effector functions including recruitment of eosinophils and suppression of T cell proliferation. Collectively, we have identified RBP-J as an essential regulator of differentiation and function of alternatively activated macrophages.

Indexed as

AnimalsCell PolarityCell ProliferationChitinEosinophilsGene Expression RegulationImmunoglobulin J Recombination Signal Sequence-Binding ProteinMacrophage ActivationMacrophagesMiceMice, TransgenicT-LymphocytesChitinImmunoglobulin J Recombination Signal Sequence-Binding ProteinRbpj protein, mousearginasechitinM2macrophagesRBP-J

Identifiers

PMID26874522
PMCPMC4791428

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Registered trials

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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.