Evidence map›Paper›PMID 29895319›Full record

ArticleArthritis research & therapy2018

GWAS-identified CCR1 and IL10 loci contribute to M1 macrophage-predominant inflammation in Behçet's disease.

Hiroto Nakano, Yohei Kirino, Mitsuhiro Takeno, Kana Higashitani, Hideto Nagai, Ryusuke Yoshimi, Yukie Yamaguchi, Ikuma Kato, Ichiro Aoki, Hideaki Nakajima

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. The roles of immune cells in Behçet's disease.Advances in rheumatology (London, England) · 2023
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Dysfunction of CCR1Frontiers in immunology · 2022
    Article
  14. Genetics in Behcet's Disease: An Update Review.Frontiers in ophthalmology · 2022
    Review
  15. Review
  16. Review
  17. Behçet syndrome.Nature reviews. Disease primers · 2021
    Review
  18. Article
  19. Article
  20. Common genetic susceptibility loci link PFAPA syndrome, Behçet's disease, and recurrent aphthous stomatitis.Proceedings of the National Academy of Sciences of the United States of America · 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

10 authors at 2 institutions in 1 country.

Hiroto NakanoYokohama City University Graduate School of Medicine, Department of Stem Cell and Immune Regulation, Yokohama, Japan.
Yohei KirinoYokohama City University Graduate School of Medicine, Department of Stem Cell and Immune Regulation, Yokohama, Japan. kirino@yokohama-cu.ac.jp.ORCID 0000-0002-9488-661X
Mitsuhiro TakenoNippon Medical School Graduate School of Medicine, Department of Allergy and Rheumatology, Tokyo, Japan.
Kana HigashitaniYokohama City University Graduate School of Medicine, Department of Stem Cell and Immune Regulation, Yokohama, Japan.
Hideto NagaiYokohama City University Graduate School of Medicine, Department of Stem Cell and Immune Regulation, Yokohama, Japan.
Ryusuke YoshimiYokohama City University Graduate School of Medicine, Department of Stem Cell and Immune Regulation, Yokohama, Japan.
Yukie YamaguchiYokohama City University Graduate School of Medicine, Department of Environmental Immuno-Dermatology, Yokohama, Japan.
Ikuma KatoYokohama City University Graduate School of Medicine, Department of Molecular Pathology, Yokohama, Japan.
Ichiro AokiYokohama City University Graduate School of Medicine, Department of Molecular Pathology, Yokohama, Japan.
Hideaki NakajimaYokohama City University Graduate School of Medicine, Department of Stem Cell and Immune Regulation, Yokohama, Japan.
Yokohama City University · JPNippon Medical School · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLow C-C chemokine receptor 1 (CCR1) and interleukin (IL)-10 expression is associated with risk of Behçet's disease (BD). The objective of the present study was to clarify the pathological roles of CCR1 and IL10 loci identified by previous BD genome-wide association studies (GWASs).

methodsM1 and M2 macrophages (Mφ) were differentiated with granulocyte-macrophage colony-stimulating factor or macrophage colony-stimulating factor (M-CSF) from peripheral monocytes of healthy control subjects (HC) and patients with BD. Expression of CD68 and CD163 was evaluated to test for Mφ polarization. CCR1 and IL-10 messenger RNA (mRNA) and protein expression was compared according to CCR1 and IL10 single-nucleotide polymorphism (SNP) genotypes. The migratory ability of M1 and M2 Mφ toward CCR1 ligand macrophage inflammatory protein (MIP)-1α was compared. The ratio of M1 and M2 Mφ in skin lesions of BD and systemic sclerosis (SSc), which was reported to be M2 Mφ-dominant, was compared. To examine the plasticity of polarized Mφ, the differentiated cells were cultured with either the same or the other culture condition.

resultsPreferential expression of CD163, CCR1, and IL-10 was found in M2 Mφ compared with M1 Mφ. M2 Mφ migrated more sensitively to low concentrations of MIP-1α than M1 Mφ did. BD-derived M1 Mφ showed higher CCR1 surface expression than HC-derived M1 Mφ did. IL10 and CCR1 mRNA expression differences were observed by GWAS-identified SNP genotypes in polarized Mφ. BD skin lesions showed M1 Mφ predominance compared with SSc skin lesions. A plasticity assay revealed that M-CSF restored IL-10 synthesis and reduced IL-6 production by M1 Mφ.

conclusionsThe present study reveals that GWAS-identified SNPs contribute to M1 Mφ-predominant inflammation in BD. Our data also suggest that the skewed Mφ polarization is correctable by immunological intervention.

Indexed as

Genome-Wide Association StudyAntigens, CDAntigens, Differentiation, MyelomonocyticBehcet SyndromeCD163 AntigenCell DifferentiationCell MovementCell PlasticityCells, CulturedChemokine CCL3Gene Expression ProfilingHumansInflammationInterleukin-10Macrophage ActivationMacrophagesAntigens, CDAntigens, Differentiation, MyelomonocyticCCR1 protein, humanCD163 AntigenChemokine CCL3Interleukin-10Receptors, CCR1Receptors, Cell SurfaceBehçet’s diseaseCCR1GWASIL-10Macrophage polarization

Identifiers

PMID29895319
PMCPMC5998575
OpenAlexW2808295578

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LicenceCC BY
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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.