Evidence map›Paper›PMID 29027226›Full record

ReviewImmunological reviews2017

Efferocytosis of dying cells differentially modulate immunological outcomes in tumor microenvironment.

Sushil Kumar, David Calianese, Raymond B Birge

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Immunological reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. A novel molecular classification based on efferocytosis-related genes for predicting clinical outcome and treatment response in acute myeloid leukemia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
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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

3 authors at 1 institution in 1 country.

Sushil KumarNew Jersey Medical School, Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers University, Newark, NJ, USA.
David CalianeseNew Jersey Medical School, Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers University, Newark, NJ, USA.
Raymond B BirgeNew Jersey Medical School, Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers University, Newark, NJ, USA.ORCID 0000-0002-0721-4672
Rutgers, The State University of New Jersey · US

Funding

Non-canonical Signal Pathway for Crk in Breast CancerR01CA165077 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI BIRGE, RAYMOND B. · 2012 to 2016
$1.7M
NCI NIH HHS R01 CA165077
6 · The paper itself

Abstract

Programmed cell death (apoptosis) is an integral part of tissue homeostasis in complex organisms, allowing for tissue turnover, repair, and renewal while simultaneously inhibiting the release of self antigens and danger signals from apoptotic cell-derived constituents that can result in immune activation, inflammation, and autoimmunity. Unlike cells in culture, the physiological fate of cells that die by apoptosis in vivo is their rapid recognition and engulfment by phagocytic cells (a process called efferocytosis). To this end, apoptotic cells express specific eat-me signals, such as externalized phosphatidylserine (PS), that are recognized in a specific context by receptors to initiate signaling pathways for engulfment. The importance of carefully regulated recognition and clearance pathways is evident in the spectrum of inflammatory and autoimmune disorders caused by defects in PS receptors and signaling molecules. However, in recent years, several additional cell death pathways have emerged, including immunogenic cell death, necroptosis, pyroptosis, and netosis that interweave different cell death pathways with distinct innate and adaptive responses from classical apoptosis that can shape long-term host immunity. In this review, we discuss the role of different cell death pathways in terms of their immune potential outcomes specifically resulting in specific cell corpse/phagocyte interactions (phagocytic synapses) that impinge on host immunity, with a main emphasis on tolerance and cancer immunotherapy.

Indexed as

ImmunityPhagocytosisAnimalsApoptosisHumansImmune TolerancePhagocytesPhosphatidylserinesSignal TransductionTumor MicroenvironmentPhosphatidylserinescell deathimmunogenic cell deathphosphatidylserinetolerancetumor immunity

Identifiers

PMID29027226
PMCPMC8359679
OpenAlexW2763913931

What OpenQuestion holds

Textmetadata
LicenceTDM
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.