Evidence map›Paper›PMID 30374349›Full record

ReviewFrontiers in immunology2018

The Impact of Invariant NKT Cells in Sterile Inflammation: The Possible Contribution of the Alarmin/Cytokine IL-33.

Maroua Haroun Ferhat, Aurélie Robin, Louise Barbier, Antoine Thierry, Jean-Marc Gombert, Alice Barbarin, André Herbelin

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 23% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Metabolic control of innate-like T cells.Nature reviews. Immunology · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Review
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  9. TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Article
  11. Review
  12. IL-33 in Rheumatic Diseases.Frontiers in medicine · 2021
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. 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

7 authors at 3 institutions in 1 country.

Maroua Haroun FerhatINSERM U1082 - IRATI Group, Poitiers, France.
Aurélie RobinINSERM U1082 - IRATI Group, Poitiers, France.
Louise BarbierService de Chirurgie Digestive, Oncologique, Endocrinienne et Transplantation Hépatique, CHU Trousseau, Université de Tours, Tours, France.
Antoine ThierryINSERM U1082 - IRATI Group, Poitiers, France.
Jean-Marc GombertINSERM U1082 - IRATI Group, Poitiers, France.
Alice BarbarinINSERM U1082 - IRATI Group, Poitiers, France.
André HerbelinINSERM U1082 - IRATI Group, Poitiers, France.
Inserm · FRCentre Hospitalier Universitaire de Tours · FRUniversité de Poitiers · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the contribution of iNKT cells to induction of sterile inflammation is now well-established, the nature of the endogenous compounds released early after cellular stress or damage that drive their activation and recruitment remains poorly understood. More precisely, iNKT cells have not been described as being reactive to endogenous non-protein damage-associated molecular-pattern molecules (DAMPs). A second subset of DAMPs, called alarmins, are tissue-derived nuclear proteins, constitutively expressed at high levels in epithelial barrier tissues and endothelial barriers. These potent immunostimulants, immediately released after tissue damage, include the alarmin IL-33. This factor has aroused interest due to its singular action as an alarmin during infectious, allergic responses and acute tissue injury, and as a cytokine, contributing to the latter resolutive/repair phase of sterile inflammation. IL-33 targets iNKT cells, inducing their recruitment in an inflammatory state, and amplifying their regulatory and effector functions. In the present review, we introduce the new concept of a biological axis of iNKT cells and IL-33, involved in alerting and controlling the immune cells in experimental models of sterile inflammation. This review will focus on acute organ injury models, especially ischemia-reperfusion injury, in the kidneys, liver and lungs, where iNKT cells and IL-33 have been presumed to mediate and/or control the injury mechanisms, and their potential relevance in human pathophysiology.

Indexed as

AlarminsAnimalsBiomarkersCytokinesHumansInflammationInterleukin-33Natural Killer T-CellsAlarminsBiomarkersCytokinesIL33 protein, humanInterleukin-33alarmin IL-33CD1d-restricted T cellsiNKTischemia reperfusionsterile inflammatory responsetissue repair

Identifiers

PMID30374349
PMCPMC6197076
OpenAlexW2897247343

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.