Evidence map›Paper›PMID 29777213›Full record

ArticleNature immunology2018

Semaphorin 6D reverse signaling controls macrophage lipid metabolism and anti-inflammatory polarization.

Sujin Kang, Yoshimitsu Nakanishi, Yoshiyuki Kioi, Daisuke Okuzaki, Tetsuya Kimura, Hyota Takamatsu, Shohei Koyama, Satoshi Nojima, Masayuki Nishide, Yoshitomo Hayama and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
–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

79 citing papers in PubMed, 1 synthesis or guideline pooled it.

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19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Sujin KangDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan. kang@imed3.med.osaka-u.ac.jp.ORCID http://orcid.org/0000-0001-5086-1405
Yoshimitsu NakanishiDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.ORCID http://orcid.org/0000-0001-6172-6364
Yoshiyuki KioiDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Suita City, Osaka, Japan.ORCID http://orcid.org/0000-0002-4552-783X
Tetsuya KimuraDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.ORCID http://orcid.org/0000-0001-6367-7818
Hyota TakamatsuDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.
Shohei KoyamaDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.
Satoshi NojimaDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.
Masayuki NishideDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.
Yoshitomo HayamaDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.
Yuhei KineharaDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.
Yasuhiro KatoDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.
Takeshi NakataniDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.
Tomomi ShimogoriRIKEN Brain Science Institute, Laboratory for Molecular Mechanisms of Thalamus Development, Saitama, Japan.
Junichi TakagiLaboratory of Protein Synthesis and Expression, Institute for Protein Research, Osaka University, Suita City, Osaka, Japan.
Toshihiko ToyofukuDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan.
Atsushi KumanogohDepartment of Immunopathology, Immunology Frontier Research Center, Osaka University, Suita City, Osaka, Japan. kumanogo@imed3.med.osaka-u.ac.jp.ORCID http://orcid.org/0000-0003-4749-7117

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polarization of macrophages into pro-inflammatory or anti-inflammatory states has distinct metabolic requirements, with mechanistic target of rapamycin (mTOR) kinase signaling playing a critical role. However, it remains unclear how mTOR regulates metabolic status to promote polarization of these cells. Here we show that an mTOR-Semaphorin 6D (Sema6D)-Peroxisome proliferator receptor γ (PPARγ) axis plays critical roles in macrophage polarization. Inhibition of mTOR or loss of Sema6D blocked anti-inflammatory macrophage polarization, concomitant with severe impairments in PPARγ expression, uptake of fatty acids, and lipid metabolic reprogramming. Macrophage expression of the receptor Plexin-A4 is responsible for Sema6D-mediated anti-inflammatory polarization. We found that a tyrosine kinase, c-Abl, which associates with the cytoplasmic region of Sema6D, is required for PPARγ expression. Furthermore, Sema6D is important for generation of intestinal resident CX3CR1

Indexed as

AnimalsCell DifferentiationColitisInflammationLipid MetabolismMacrophagesMiceMice, Inbred C57BLPPAR gammaSemaphorinsSignal TransductionTOR Serine-Threonine KinasesmTOR protein, mousePPAR gammaSema6d protein, mouseSemaphorinsTOR Serine-Threonine Kinases

Identifiers

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.