Evidence map›Paper›PMID 23515163›Full record

ArticleNature2013

Critical role of Trib1 in differentiation of tissue-resident M2-like macrophages.

Takashi Satoh, Hiroyasu Kidoya, Hisamichi Naito, Masahiro Yamamoto, Naoki Takemura, Katsuhiro Nakagawa, Yoshichika Yoshioka, Eiichi Morii, Nobuyuki Takakura, Osamu Takeuchi and 1 more

Abstract read
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In one paragraph

Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
165citing papers in PubMed, 2 pooled it
18.3field-weighted citation impact, top 1% 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

165 citing papers in PubMed, 2 syntheses or guidelines pooled it, 299 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Adipose-Tissue Macrophage Diversity and Functions.International journal of molecular sciences · 2026
    Review
  6. Article
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  9. Article
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  13. First reportedLeukemia research reports · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

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

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

11 authors at 2 institutions in 1 country.

Takashi SatohLaboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.
Hiroyasu Kidoya
Hisamichi Naito
Masahiro Yamamoto
Naoki Takemura
Katsuhiro Nakagawa
Yoshichika Yoshioka
Eiichi Morii
Nobuyuki Takakura
Osamu Takeuchi
Shizuo Akira
Osaka University · JPKyoto University · JP

Funding

Sequencing CoreP01AI070167 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI BEUTLER, BRUCE A · 2006 to 2016
$27.2M
NIAID NIH HHS P01 AI070167
6 · The paper itself

Abstract

Macrophages consist of at least two subgroups, M1 and M2 (refs 1-3). Whereas M1 macrophages are proinflammatory and have a central role in host defence against bacterial and viral infections, M2 macrophages are associated with responses to anti-inflammatory reactions, helminth infection, tissue remodelling, fibrosis and tumour progression. Trib1 is an adaptor protein involved in protein degradation by interacting with COP1 ubiquitin ligase. Genome-wide association studies in humans have implicated TRIB1 in lipid metabolism. Here we show that Trib1 is critical for the differentiation of F4/80(+)MR(+) tissue-resident macrophages--that share characteristics with M2 macrophages (which we term M2-like macrophages)--and eosinophils but not for the differentiation of M1 myeloid cells. Trib1 deficiency results in a severe reduction of M2-like macrophages in various organs, including bone marrow, spleen, lung and adipose tissues. Aberrant expression of C/EBPα in Trib1-deficient bone marrow cells is responsible for the defects in macrophage differentiation. Unexpectedly, mice lacking Trib1 in haematopoietic cells show diminished adipose tissue mass accompanied by evidence of increased lipolysis, even when fed a normal diet. Supplementation of M2-like macrophages rescues the pathophysiology, indicating that a lack of these macrophages is the cause of lipolysis. In response to a high-fat diet, mice lacking Trib1 in haematopoietic cells develop hypertriglyceridaemia and insulin resistance, together with increased proinflammatory cytokine gene induction. Collectively, these results demonstrate that Trib1 is critical for adipose tissue maintenance and suppression of metabolic disorders by controlling the differentiation of tissue-resident M2-like macrophages.

Indexed as

Cell DifferentiationAdipose TissueAnimalsBone Marrow CellsCCAAT-Enhancer-Binding Protein-alphaCell CountCell Cycle ProteinsCytokinesDiet, High-FatEosinophilsFemaleHypertriglyceridemiaInflammation MediatorsInsulin ResistanceIntracellular Signaling Peptides and ProteinsLipodystrophyCCAAT-Enhancer-Binding Protein-alphaCell Cycle ProteinsCytokinesInflammation MediatorsIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesTRB3 protein, mouseTrib1 protein, mousetribbles 2 protein, mouseUbiquitin

Identifiers

PMID23515163
OpenAlexW2074340664

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.