Evidence map›Paper›PMID 35003105›Full record

ArticleFrontiers in immunology2021

Extracellular ATP Limits Homeostatic T Cell Migration Within Lymph Nodes.

Daichi Kobayashi, Yuki Sugiura, Eiji Umemoto, Akira Takeda, Hisashi Ueta, Haruko Hayasaka, Shinsuke Matsuzaki, Tomoya Katakai, Makoto Suematsu, Itaru Hamachi and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
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  8. Physiologic roles of P2 receptors in leukocytes.Journal of leukocyte biology · 2022
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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

14 authors at 9 institutions in 2 countries.

Daichi KobayashiDepartment of Immunology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Yuki SugiuraDepartment of Biochemistry, Keio University School of Medicine, Tokyo, Japan.
Eiji UmemotoLaboratory of Microbiology and Immunology, University of Shizuoka, Shizuoka, Japan.
Akira TakedaMediCity Research Laboratory, University of Turku, Turku, Finland.
Hisashi UetaDepartment of Anatomy, School of Medicine, Dokkyo Medical University, Tochigi, Japan.
Haruko HayasakaLaboratory of Immune Molecular Function, Faculty of Science and Engineering, Kindai University, Higashi-Osaka, Japan.
Shinsuke MatsuzakiDepartment of Pharmacology, Wakayama Medical University, Wakayama, Japan.
Tomoya KatakaiDepartment of Immunology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Makoto SuematsuDepartment of Biochemistry, Keio University School of Medicine, Tokyo, Japan.
Itaru HamachiDepartment of Synthetic Chemistry and Biological Chemistry, Graduate School of Engineering, Kyoto University, Kyoto, Japan.
Gennady G YegutkinMediCity Research Laboratory, University of Turku, Turku, Finland.
Marko SalmiMediCity Research Laboratory, University of Turku, Turku, Finland.
Sirpa JalkanenMediCity Research Laboratory, University of Turku, Turku, Finland.
Masayuki MiyasakaMediCity Research Laboratory, University of Turku, Turku, Finland.
University of Turku · FIKeio University · JPDokkyo Medical University · JPKindai University · JPKyoto University · JPMorinomiya University of Medical Sciences · JPNiigata University · JPUniversity of Shizuoka · JPWakayama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Whereas adenosine 5'-triphosphate (ATP) is the major energy source in cells, extracellular ATP (eATP) released from activated/damaged cells is widely thought to represent a potent damage-associated molecular pattern that promotes inflammatory responses. Here, we provide suggestive evidence that eATP is constitutively produced in the uninflamed lymph node (LN) paracortex by naïve T cells responding to C-C chemokine receptor type 7 (CCR7) ligand chemokines. Consistently, eATP was markedly reduced in naïve T cell-depleted LNs, including those of nude mice, CCR7-deficient mice, and mice subjected to the interruption of the afferent lymphatics in local LNs. Stimulation with a CCR7 ligand chemokine, CCL19, induced ATP release from LN cells, which inhibited CCR7-dependent lymphocyte migration

Indexed as

Adenosine TriphosphateAnimalsCell MovementIntravital MicroscopyLymph NodesMiceModels, AnimalPurinergic P2X Receptor AntagonistsPyridinesRatsReceptors, CCR7Receptors, Purinergic P2X7TetrazolesT-Lymphocytes3-(5-(2,3-dichlorophenyl)-1H-tetrazol-1-yl)methylpyridineAdenosine TriphosphateCcr7 protein, mouseP2rx7 protein, mousePurinergic P2X Receptor AntagonistsPyridinesReceptors, CCR7Receptors, Purinergic P2X7Tetrazolesadenosine 5’-triphosphate (ATP)cell migrationchemokineslymph nodes (LNs)T cells

Identifiers

PMID35003105
PMCPMC8728011
OpenAlexW4200541633

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.