Evidence map›Paper›PMID 33133068›Full record

ReviewFrontiers in immunology2020

Mitochondria Synergize With P2 Receptors to Regulate Human T Cell Function.

Carola Ledderose, Wolfgang G Junger

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Hemoglobin as an oxygen gasoreceptor.Acta biochimica Polonica · 2025
    Review
  8. Article
  9. Time-resolved role of P2X4 and P2X7 during CD8Frontiers in immunology · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Antimicrobial Activity of the Peptide LfcinB15 againstJournal of fungi (Basel, Switzerland) · 2021
    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

2 authors at 2 institutions in 1 country.

Carola LedderoseDepartment of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, United States.
Wolfgang G JungerDepartment of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, United States.
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

Purinergic regulation of T cellsR01GM051477 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JUNGER, WOLFGANG G · 2003 to 2016
$2.5M
Metabolic and purinergic immune regulationR35GM136429 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JUNGER, WOLFGANG G · 2020 to 2024
$2.3M
Role of purinergic signaling in pediatric multi-organ failureR01HD098363 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JUNGER, WOLFGANG G · 2019 to 2023
$2.0M
Autocrine regulation of neutrophil chemotaxisR01GM116162 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI JUNGER, WOLFGANG G · 2015 to 2018
$1.6M
Harvard Trauma Inflammation Training ProgramT32GM103702 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI JUNGER, WOLFGANG G · 2013 to 2017
$922k
NICHD NIH HHS R01 HD098363NIGMS NIH HHS R01 GM051477NIGMS NIH HHS R01 GM116162NIGMS NIH HHS R35 GM136429NIGMS NIH HHS T32 GM103702
6 · The paper itself

Abstract

Intracellular ATP is the universal energy carrier that fuels many cellular processes. However, immune cells can also release a portion of their ATP into the extracellular space. There, ATP activates purinergic receptors that mediate autocrine and paracrine signaling events needed for the initiation, modulation, and termination of cell functions. Mitochondria contribute to these processes by producing ATP that is released. Here, we summarize the synergistic interplay between mitochondria and purinergic signaling that regulates T cell functions. Specifically, we discuss how mitochondria interact with P2X1, P2X4, and P2Y11 receptors to regulate T cell metabolism, cell migration, and antigen recognition. These mitochondrial and purinergic signaling mechanisms are indispensable for host immune defense. However, they also represent an Achilles heel that can render the host susceptible to infections and inflammatory disorders. Hypoxia and mitochondrial dysfunction deflate the purinergic signaling mechanisms that regulate T cells, while inflammation and tissue damage generate excessive systemic ATP levels that distort autocrine purinergic signaling and impair T cell function. An improved understanding of the metabolic and purinergic signaling mechanisms that regulate T cells may lead to novel strategies for the diagnosis and treatment of infectious and inflammatory diseases.

Indexed as

ImmunomodulationAdenosine TriphosphateAnimalsCell CommunicationCell CycleCell MovementEnergy MetabolismHumansImmunological SynapsesMitochondriaReceptors, Purinergic P2XSignal TransductionT-LymphocytesAdenosine TriphosphateReceptors, Purinergic P2XinflammationmitochondriaP2X1P2X4P2Y11

Identifiers

PMID33133068
PMCPMC7550529
OpenAlexW3091024854

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.