Evidence map›Paper›PMID 26734458›Full record

ArticleImmunity, inflammation and disease2015

A2B adenosine receptor activation switches differentiation of bone marrow cells to a CD11c(+)Gr-1(+) dendritic cell subset that promotes the Th17 response.

Dongchun Liang, Aijun Zuo, Hui Shao, Mingjiazi Chen, Henry J Kaplan, Deming Sun

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Adenosine and Inflammation: Here, There and Everywhere.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Adenosine Signaling in Autoimmune Disorders.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  10. Review
  11. CD73Frontiers in immunology · 2020
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Dendritic Cells and Cancer Immunity.Trends in immunology · 2016
    Review
  18. Tumor-derived factors modulating dendritic cell function.Cancer immunology, immunotherapy : CII · 2016
    Review
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Dongchun LiangDepartment of Ophthalmology of the University of California Los Angeles Doheny Eye Institute California 90033 USA.
Aijun ZuoDepartment of Ophthalmology of the University of California Los Angeles Doheny Eye Institute California 90033 USA.
Hui ShaoDepartment of Ophthalmology and Visual Sciences Kentucky Lions Eye Center University of Louisville Louisville Kentucky 40202 USA.
Mingjiazi ChenDepartment of Ophthalmology of the University of California Los Angeles Doheny Eye Institute California 90033 USA.
Henry J KaplanDepartment of Ophthalmology and Visual Sciences Kentucky Lions Eye Center University of Louisville Louisville Kentucky 40202 USA.
Deming SunDepartment of Ophthalmology of the University of California Los Angeles Doheny Eye Institute California 90033 USA.
University of California, Los Angeles · USUniversity of Louisville · US

Funding

Role of IL-17+ Autoreactive T Cells in Experimental Autoimmune Uveitis (EAU)R01EY018827 · NEI · DOHENY EYE INSTITUTE · PI SUN, DEMING · 2009 to 2023
$4.8M
Regulation by Gammadelta T Cells of Autoimmune Uveitis (EAU)R01EY022403 · NEI · DOHENY EYE INSTITUTE · PI SUN, DEMING · 2012 to 2015
$1.6M
NEI NIH HHS R01 EY018827NEI NIH HHS R01 EY022403
6 · The paper itself

Abstract

Adenosine is one of the major molecules associated with inflammation. We have previously reported that an adenosine receptor (AR) agonist has an enhancing effect on Th17 autoimmune responses, even though it suppressed Th1 responses. To determine the mechanism involved, we have examined the effect of AR agonists on mouse bone marrow dendritic cell (BMDC) differentiation and function. We show that mouse bone marrow cells (BMCs) differentiated into CD11c(+)Gr-1(+) dentritic cells (DCs) when cultured in granulocyte macrophage colony-stimulating factor (GM-CSF)-containing medium containing an AR agonist. The non-selective AR agonist NECA and an A2BR-specific agonist had a similar effect, and the effect of NECA could be blocked by an A2BR-specific antagonist. Unlike CD11c(+)Gr-1(-) BMDCs, which have a greater stimulatory effect on Th1 T cells than Th17 cells, CD11c(+)Gr-1(+) BMDCs had a greater stimulatory effect on Th17 autoreactive T cells than on Th1 autoreactive T cells and this effect depended on γδ T cell activation.

Indexed as

Adenosine receptorsautoimmunityexperimental autoimmune uveitisIL‐17Th17uveitisγδ T cells

Identifiers

PMID26734458
PMCPMC4693722
OpenAlexW2147330402

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.