Evidence map›Paper›PMID 23225885›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Blocking A2B adenosine receptor alleviates pathogenesis of experimental autoimmune encephalomyelitis via inhibition of IL-6 production and Th17 differentiation.

Wei Wei, Changsheng Du, Jie Lv, Guixian Zhao, Zhenxin Li, Zhiying Wu, György Haskó, Xin Xie

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Protection From Demyelination by the Novel Adenosine Dual AJournal of cellular and molecular medicine · 2025
    Article
  5. Review
  6. APurinergic signalling · 2025
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  7. Intrinsic ecto-5'-Nucleotidase/AMolecular neurobiology · 2024
    Article
  8. Article
  9. Review
  10. Review
  11. Adenosine-mediated immune responses in inflammatory bowel disease.Frontiers in cell and developmental biology · 2024
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review

1 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

8 authors at 5 institutions in 2 countries.

Wei WeiLaboratory of Receptor-Based Bio-medicine, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China.
Changsheng Du
Jie Lv
Guixian Zhao
Zhenxin Li
Zhiying Wu
György Haskó
Xin Xie
Tongji University · CNFudan University · CNObstetrics and Gynecology Hospital of Fudan University · CNShanghai Institute of Materia Medica · CNUniversity Hospital, Newark · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adenosine is a key endogenous signaling molecule that regulates immune responses. A(2B) adenosine receptor (AR) is a relatively low-affinity receptor for adenosine, and the activation of A(2B)AR is believed to require pathological level of adenosine that is associated with ischemia, inflammation, trauma, or other types of stress. The role of A(2B)AR in the pathogenesis of multiple sclerosis (MS) is still unclear. In this study, we discovered that A(2B)AR was upregulated both in the peripheral blood leukocytes of MS patients and the peripheral lymphoid tissues of experimental autoimmune encephalomyelitis (EAE) mice. A(2B)AR-specific antagonists, CVT-6883 and MRS-1754, alleviated the clinical symptoms of EAE and protected the CNS from immune damage. A(2B)AR-knockout mice also developed less severe EAE. Further study indicated that blocking or deleting A(2B)AR inhibited Th17 cell differentiation by blocking IL-6 production from APCs such as dendritic cells. In dendritic cells, A(2B)AR was also upregulated during the development of EAE. CVT-6883 and genetic deletion of A(2B)AR significantly reduced adenosine-mediated IL-6 production. The phospholipase Cβ-protein kinase C and p38 MAPK pathways were found to be involved in the A(2B)AR-mediated IL-6 production. Our findings not only revealed the pathological role of A(2B)AR in EAE, but also suggested that this receptor might be a new therapeutic target for the development of anti-MS drugs.

Indexed as

Interleukin-6 InhibitorsAdultAnimalsCell DifferentiationCells, CulturedCoculture TechniquesEncephalomyelitis, Autoimmune, ExperimentalFemaleGrowth InhibitorsHumansInterleukin-6MaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedGrowth InhibitorsIL6 protein, humanInterleukin-6Interleukin-6 Inhibitorsinterleukin-6, mouseReceptor, Adenosine A2B

Identifiers

PMID23225885
PMCPMC3539684
OpenAlexW2112926941

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.