Evidence map›Paper›PMID 25613374›Full record

ArticleCell death and differentiation2015

Necroptosis suppresses inflammation via termination of TNF- or LPS-induced cytokine and chemokine production.

C J Kearney, S P Cullen, G A Tynan, C M Henry, D Clancy, E C Lavelle, S J Martin

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 132 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. PeerJ · 2026
    Article
  8. Article
  9. Induced necroptosis limitsInfection and immunity · 2025
    Article
  10. Review
  11. Neutrophil death-more than meets the eye.Experimental hematology · 2025
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. The emerging roles of necroptosis in skeletal muscle health and disease.Pflugers Archiv : European journal of physiology · 2024
    Review
  17. Article
  18. Review
  19. Dying to Defend: Neutrophil Death Pathways and their Implications in Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  20. Necroptosis in bacterial infections.Frontiers in immunology · 2024
    Review

27 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

C J KearneyMolecular Cell Biology Laboratory, Department of Genetics, The Smurfit Institute, Trinity College, Dublin D2, Ireland.
S P Cullen1] Molecular Cell Biology Laboratory, Department of Genetics, The Smurfit Institute, Trinity College, Dublin D2, Ireland [2] Immunology Research Centre, Trinity College, Dublin D2, Ireland.
G A TynanAdjuvant Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College, Dublin D2, Ireland.
C M HenryMolecular Cell Biology Laboratory, Department of Genetics, The Smurfit Institute, Trinity College, Dublin D2, Ireland.
D ClancyMolecular Cell Biology Laboratory, Department of Genetics, The Smurfit Institute, Trinity College, Dublin D2, Ireland.
E C Lavelle1] Immunology Research Centre, Trinity College, Dublin D2, Ireland [2] Adjuvant Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College, Dublin D2, Ireland.
S J Martin1] Molecular Cell Biology Laboratory, Department of Genetics, The Smurfit Institute, Trinity College, Dublin D2, Ireland [2] Immunology Research Centre, Trinity College, Dublin D2, Ireland.
Trinity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TNF promotes a regulated form of necrosis, called necroptosis, upon inhibition of caspase activity in cells expressing RIPK3. Because necrosis is generally more pro-inflammatory than apoptosis, it is widely presumed that TNF-induced necroptosis may be detrimental in vivo due to excessive inflammation. However, because TNF is intrinsically highly pro-inflammatory, due to its ability to trigger the production of multiple cytokines and chemokines, rapid cell death via necroptosis may blunt rather than enhance TNF-induced inflammation. Here we show that TNF-induced necroptosis potently suppressed the production of multiple TNF-induced pro-inflammatory factors due to RIPK3-dependent cell death. Similarly, necroptosis also suppressed LPS-induced pro-inflammatory cytokine production. Consistent with these observations, supernatants from TNF-stimulated cells were more pro-inflammatory than those from TNF-induced necroptotic cells in vivo. Thus necroptosis attenuates TNF- and LPS-driven inflammation, which may benefit intracellular pathogens that evoke this mode of cell death by suppressing host immune responses.

Indexed as

ApoptosisCell LineChemokinesCytokinesHumansLipopolysaccharidesProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesToll-Like Receptor 4Tumor Necrosis Factor-alphaChemokinesCytokinesLipopolysaccharidesMLKL protein, humanProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humanToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID25613374
PMCPMC4495357
OpenAlexW2029673642

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.