Evidence map›Paper›PMID 31944217›Full record

ArticleThe Journal of experimental medicine2020

The colonic macrophage transcription factor RBP-J orchestrates intestinal immunity against bacterial pathogens.

Lan Kang, Xiang Zhang, Liangliang Ji, Tiantian Kou, Sinead M Smith, Baohong Zhao, Xiaohuan Guo, Inés Pineda-Torra, Li Wu, Xiaoyu Hu

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

10 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    Review
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  6. Article
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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

10 authors at 5 institutions in 4 countries.

Lan KangInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Xiang ZhangInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Liangliang JiInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Tiantian KouInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Sinead M SmithArthritis and Tissue Degeneration Program and the David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY.
Baohong ZhaoArthritis and Tissue Degeneration Program and the David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY.
Xiaohuan GuoInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Inés Pineda-TorraDivision of Medicine, Centre for Cardiometabolic Medicine, University College of London, London, UK.
Li WuInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Xiaoyu HuInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Center for Life Sciences · CNHospital for Special Surgery · USNational Institute of Biological Sciences, Beijing · CNTsinghua University · CNUniversity College London · GB

Funding

British Heart Foundation PG/13/10/30000
6 · The paper itself

Abstract

Macrophages play pleiotropic roles in maintaining the balance between immune tolerance and inflammatory responses in the gut. Here, we identified transcription factor RBP-J as a crucial regulator of colonic macrophage-mediated immune responses against the enteric pathogen Citrobacter rodentium. In the immune response phase, RBP-J promoted pathogen clearance by enhancing intestinal macrophage-elicited Th17 cell immune responses, which was achieved by maintenance of C/EBPβ-dependent IL-6 production by overcoming miRNA-17∼92-mediated suppressive effects. RBP-J deficiency-associated phenotypes could be genetically corrected by further deleting miRNA-17∼92 in macrophages. In the late phase, noneradicated pathogens in RBP-J KO mice recruited abundant IL-1β-expressing CD64+Ly6C+ colonic macrophages and thereby promoted persistence of ILC3-derived IL-22 to compensate for the impaired innate and adaptive immune responses, leading to ultimate clearance of pathogens. These results demonstrated that colonic macrophage-intrinsic RBP-J dynamically orchestrates intestinal immunity against pathogen infections by interfacing with key immune cells of T and innate lymphoid cell lineages.

Indexed as

AnimalsCitrobacter rodentiumColonEnterobacteriaceae InfectionsFemaleGene Knockout TechniquesHost-Pathogen InteractionsImmunity, HumoralImmunity, InnateImmunoglobulin J Recombination Signal Sequence-Binding ProteinInterleukinsMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutImmunoglobulin J Recombination Signal Sequence-Binding ProteinInterleukinsMicroRNAsMirn17 microRNA, mouseRbpj protein, mouse

Identifiers

PMID31944217
PMCPMC7144519
OpenAlexW3000394566

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.