Evidence map›Paper›PMID 21586357›Full record

ReviewAdvances in pharmacology (San Diego, Calif.)2011

Regulation of leukocyte function by adenosine receptors.

Joel Linden

Abstract readReview
In one paragraph

Review in Advances in pharmacology (San Diego, Calif.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.1field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 57 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Non-Nucleoside Agonists of the Adenosine Receptors: An Overview.Pharmaceuticals (Basel, Switzerland) · 2019
    Review
  10. Adenosine AMolecular medicine (Cambridge, Mass.) · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Schwann Cells Metabolize Extracellular 2',3'-cAMP to 2'-AMP.The Journal of pharmacology and experimental therapeutics · 2015
    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

1 author at 1 institution in 1 country.

Joel LindenDivision of Inflammation Biology, La Jolla Institute of Allergy and Immunology, California, USA.
La Jolla Institute for Immunology · US

Funding

Targeted CEU Imaging of Atherosclerosis and AngiogenesisR01HL078610 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI LINDNER, JONATHAN R · 2004 to 2022
$6.8M
Biomarkers of Inflammation and Vaso-occlusion in Sickle Cell DiseaseR01HL111969 · NHLBI · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI FIELD, JOSHUA JEFFREY, LINDEN, JOEL M. · 2012 to 2016
$4.0M
ALLOSTERIC ENHANCEMENT OF ADENOSINE RECEPTORSR01HL056111 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI LINDEN, JOEL M. · 1996 to 2009
$2.9M
NHLBI NIH HHS R01 HL056111NHLBI NIH HHS R01 HL078610NHLBI NIH HHS R01 HL111969
6 · The paper itself

Abstract

The immune system responds to cues in the microenvironment to make acute and chronic adaptations in response to inflammation and injury. Locally produced purine nucleotides and adenosine provide receptor-mediated signaling to all bone-marrow derived cells of the immune system to modulate their responses. This review summarizes recent advances in our understanding of the effects of adenosine signaling through G protein-coupled adenosine receptors on cells of the immune system. Adenosine A(2A) receptors (A(2A)Rs) have a generally suppressive effect on the activation of immune cells. Moreover, their transcription is strongly induced by signals that activate macrophages or dendritic cells through toll-like receptors, or T cells through T cell receptors. A(2A)R induction is responsible for producing a gradual dissipation of inflammatory responses. A(2A)R activation is particularly effective in limiting the activation of invariant NKT (iNKT) cells that play a central role in acute reperfusion injury. A(2A) agonists have clinical promise for the treatment of vaso-occlusive tissue injury. Blockade of A(2A) receptors may be useful to enhance immune-mediated killing of cancer cells. A(2B)R expression also is transcriptionally regulated by hypoxia, cytokines, and oxygen radicals. Acute A(2B)R activation attenuates the production of proinflammatory cytokines from macrophages, but sustained activation facilitates macrophage and dendritic cell remodeling and the production of acute phase proteins and angiogenic factors that may participate in evoking insulin resistance and tissue fibrosis. A(2B)R activation also influences macrophage and neutrophil function by influencing expression of the anti-inflammatory netrin receptor, UNC5B. The therapeutic significance of adenosine-mediated effects on the immune system is discussed.

Indexed as

AdenosineAnimalsDiseaseHumansImmunityLeukocytesReceptors, Purinergic P1Signal TransductionAdenosineReceptors, Purinergic P1

Identifiers

PMID21586357
PMCPMC4211873
OpenAlexW1523828834

What OpenQuestion holds

Textmetadata
LicenceTDM
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.