Evidence map›Paper›PMID 30185656›Full record

ArticleJCI insight2018

Induction of antiinflammatory purinergic signaling in activated human iNKT cells.

Jennifer C Yu, Gene Lin, Joshua J Field, Joel Linden

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Adenosine-mediated immune responses in inflammatory bowel disease.Frontiers in cell and developmental biology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Ectonucleotidase Modulation of Lymphocyte Function in Gut and Liver.Frontiers in cell and developmental biology · 2020
    Review
  10. Review
  11. Review
  12. 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

4 authors at 2 institutions in 1 country.

Jennifer C YuDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology La Jolla, California, USA.
Gene LinDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology La Jolla, California, USA.
Joshua J FieldBloodCenter of Wisconsin, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Joel LindenDivision of Developmental Immunology, La Jolla Institute for Allergy and Immunology La Jolla, California, USA.
La Jolla Institute for Immunology · USMedical College of Wisconsin · US

Funding

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
NHLBI NIH HHS R01 HL111969
6 · The paper itself

Abstract

Invariant natural killer T (iNKT) cells are activated at sites of local tissue injury, or globally during vaso-occlusive episodes of sickle cell disease (SCD). Tissue damage stimulates production of CD1d-restricted lipid antigens that activate iNKT cells to produce Th1- and Th2-type cytokines. Here, we show that circulating iNKT cells in SCD patients express elevated levels of the ectonucleoside triphosphate diphosphosphohydrolase, CD39, as well the adenosine A2A receptor (A2AR). We also investigated the effects of stimulating cultured human iNKT cells on the expression of genes involved in the regulation of purinergic signaling. iNKT cell stimulation caused induction of ADORA2A, P2RX7, CD38, CD39, ENPP1, CD73, PANX1, and ENT1. Transcription of ADA, which degrades adenosine, was reduced. Induction of CD39 mRNA was associated with increased ecto-ATPase activity on iNKT cells that was blocked by POM1. Exposure of iNKT cells to A2AR agonists during stimulation reduced production of IFN-γ and enhanced production of IL-13 and CD39. Based on these findings, we define "purinergic Th2-type cytokine bias" as an antiinflammatory purinergic response to iNKT cell stimulation resulting from changes in the transcription of several genes involved in purine release, extracellular metabolism, and signaling.

Indexed as

5'-NucleotidaseADP-ribosyl Cyclase 1Anemia, Sickle CellAntigens, CD1dApyraseConnexinsCytokinesEquilibrative Nucleoside Transporter 1GPI-Linked ProteinsHumansImmunity, InnateInterleukin-13Natural Killer T-CellsNerve Tissue ProteinsPhosphoric Diester HydrolasesPurinergic Agents5'-NucleotidaseADORA2A protein, humanADP-ribosyl Cyclase 1Antigens, CD1dApyraseConnexinsCytokinesectonucleotide pyrophosphatase phosphodiesterase 1ENTPD1 protein, humanEquilibrative Nucleoside Transporter 1GPI-Linked ProteinsInterleukin-13Nerve Tissue ProteinsNT5E protein, humanP2RX7 protein, humanPANX1 protein, humanPhosphoric Diester HydrolasespurinePurinergic AgentsPurinesPyrophosphatasesReceptor, Adenosine A2AReceptors, Purinergic P2X7SLC29A1 protein, humanTranscription FactorsImmunologyInflammationInnate immunityNK T cells

Identifiers

PMID30185656
PMCPMC6171811
OpenAlexW2890581073

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.