Evidence map›Paper›PMID 33013906›Full record

ArticleFrontiers in immunology2020

Semaphorin 4D Induces an Imbalance of Th17/Treg Cells by Activating the Aryl Hydrocarbon Receptor in Ankylosing Spondylitis.

Jianmin Xie, Zitao Wang, Wen Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  15. Uncovering the Underworld of Axial Spondyloarthritis.International journal of molecular sciences · 2023
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Jianmin XieDepartment of Rheumatology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zitao WangDepartment of Rheumatology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wen WangDepartment of Rheumatology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Second Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: Semaphorin 4D (Sema4D) is constitutively expressed on T cells and osteoclasts, and regulates T cell proliferation and bone remodeling. In addition, several studies have shown that Sema4D is involved in the pathogenesis of autoimmunity. We undertook this study to investigate the mechanism by which Sema4D affects the pathogenic progress of ankylosing spondylitis (AS). Methods: Soluble Sema4D (sSema4D) levels in serum were analyzed by enzyme-linked immunosorbent assay. The cell surface levels and transcripts of Sema4D were evaluated in CD4 + and CD19 + cells from the AS patients and healthy individuals. The mRNA expression levels were assessed by quantitative polymerase chain reaction (qPCR). The proportions of Treg cells and IL-17-producing T-cells (Th17 cells) differentiated from CD4 + T cells were analyzed by flow cytometric analysis. The aryl hydrocarbon receptor (AhR) agonistic effect of Sema4D was detected by analyzing the activation of downstream signaling pathways and target genes using Luciferase and EROD assay. Results: Levels of sSema4D were elevated in both serum from AS patients, and clinical features markers were correlated with serum sSema4D levels. Sema4D facilitated CD4 + T cells proliferation and Th17 cells differentiation and inhibited Treg cells differentiation by enhancing RORγt expression and reducing Foxp3 expression, with increasing expression and secretion of IL-17 and IL-22. It induced the expression and activity of AhR target gene CYP1A1 and XRE reporter activity Conclusion: These findings indicate that Sema4D as a potent activator of T cells in the immune response contributes to the inflammation of AS by inducing imbalance in Th17 and Treg cell populations in an AhR-dependent manner, suggesting it is a crucial participant in AS pathogenesis.

Indexed as

CD4 Lymphocyte CountTh17 CellsT-Lymphocytes, RegulatoryAdultAntigens, CDCell DifferentiationCytochrome P-450 CYP1A1FemaleForkhead Transcription FactorsGene Expression RegulationHumansInterleukin-17Lymphocyte ActivationMaleMiddle AgedNuclear Receptor Subfamily 1, Group F, Member 3Antigens, CDCD100 antigenCYP1A1 protein, humanCytochrome P-450 CYP1A1Forkhead Transcription FactorsFOXP3 protein, humanInterleukin-17Nuclear Receptor Subfamily 1, Group F, Member 3Receptors, Aryl HydrocarbonReceptors, Interleukin-17RNA, MessengerRORC protein, humanSemaphorinsankylosing spondylitisaryl hydrocarbon receptorssemaphorin 4DTh17Treg

Identifiers

PMID33013906
PMCPMC7505929
OpenAlexW3087951701

What OpenQuestion holds

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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.