Evidence map›Paper›PMID 25145756›Full record

ReviewNature reviews. Immunology2014

A long-awaited merger of the pathways mediating host defence and programmed cell death.

J Magarian Blander

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
8.4field-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

78 citing papers in PubMed, 120 citations in OpenAlex.

  1. Trial
  2. Review
  3. Toll like receptor 4 (TLR4) in neuroinflammation: From acute hemorrhagic stroke to chronic neurodegeneration.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Outcomes of RIP Kinase Signaling During Neuroinvasive Viral Infection.Current topics in microbiology and immunology · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Protein Kinase-Mediated Decision Between the Life and Death.Advances in experimental medicine and biology · 2021
    Article

18 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

1 author at 1 institution in 1 country.

J Magarian BlanderImmunology Institute and Tisch Cancer Institute, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.
Tisch Hospital · US

Funding

THE ROLE OF ICSBP IN MUCOSAL IMMUNE RESPONSEP01DK072201 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HARPAZ, NOAM · 2006 to 2015
$14.6M
Control of protective immunity by innate pathways sensing bacterial viabilityR01AI095245 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BLANDER, JULIE MAGARIAN · 2012 to 2015
$1.7M
Innate Immune Sensing of Microbial ViabilityR21AI080959 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI BLANDER, JULIE MAGARIAN · 2009 to 2010
$466k
NIAID NIH HHS AI095245NIAID NIH HHS R01 AI095245NIAID NIH HHS R21 AI080959NIDDK NIH HHS DK072201NIDDK NIH HHS P01 DK072201
6 · The paper itself

Abstract

Historically, cell death and inflammation have been closely linked, but the necessary divergence of the fields in the past few decades has enriched our molecular understanding of the signalling pathways that mediate various programmes of cell death and multiple types of inflammatory responses. The fields have now come together again demonstrating a surprising level of integration. Intimate interconnections at multiple levels are revealed between the cell death and inflammatory signal transduction pathways that are mobilized in response to the engagement of pattern recognition receptors during microbial infection. Molecules such as receptor-interacting protein kinase 1 (RIPK1), RIPK3, FAS-associated death domain protein (FADD), FLICE-like inhibitory protein (FLIP) and caspase 8 - which are associated with different forms of cell death - are incorporated into compatible and exceedingly dynamic Toll-like receptor, NOD-like receptor and RIG-I-like receptor signalling modules. These signalling modules have a high capacity to switch from inflammation to cell death, or a programmed execution of both, all in an orchestrated battle for host defence and survival.

Indexed as

InflammationAdaptor Proteins, Vesicular TransportAnimalsApoptosisAutophagyCarrier ProteinsCaspasesFas-Associated Death Domain ProteinGram-Negative BacteriaGram-Negative Bacterial InfectionsHumansMiceNLR Family, Pyrin Domain-Containing 3 ProteinReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionToll-Like ReceptorsAdaptor Proteins, Vesicular TransportCarrier ProteinsCaspasesFas-Associated Death Domain ProteinNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanRIPK3 protein, humanTICAM1 protein, humanToll-Like Receptors

Identifiers

PMID25145756
OpenAlexW1969087061

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.