Evidence map›Paper›PMID 28847720›Full record

ReviewJournal of molecular biology2017

LC3-Associated Phagocytosis and Inflammation.

Bradlee L Heckmann, Emilio Boada-Romero, Larissa D Cunha, Joelle Magne, Douglas R Green

Abstract readReview
In one paragraph

Review in Journal of molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
172citing papers in PubMed, 2 pooled it
10.8field-weighted citation impact, top 1% 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

172 citing papers in PubMed, 2 syntheses or guidelines pooled it, 262 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Emerging mechanisms of ATG8-independent non-canonical autophagy.Journal of physiology and biochemistry · 2026
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  8. From lipid overload to autophagy collapse: how lipid dysregulation drives chronic inflammation and metabolic disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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112 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

5 authors at 1 institution in 1 country.

Bradlee L HeckmannDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, United States.
Emilio Boada-RomeroDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, United States.
Larissa D CunhaDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, United States.
Joelle MagneDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, United States.
Douglas R GreenDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, United States. Electronic address: douglas.green@stjude.org.
St. Jude Children's Research Hospital · US

Funding

Non-canonical functions of autophagy proteinsR01AI040646 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI GREEN, DOUGLAS R. · 1997 to 2023
$8.6M
Regulation of microglial induced inflammation by non-canonical autophagyF32AI138492 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI HECKMANN, BRADLEE L · 2018 to 2020
$130k
NCI NIH HHS L40 CA231423NIAID NIH HHS F32 AI138492NIAID NIH HHS R01 AI040646
6 · The paper itself

Abstract

LC3-associated phagocytosis (LAP) is a novel form of non-canonical autophagy where LC3 (microtubule-associated protein 1A/1B-light chain 3) is conjugated to phagosome membranes using a portion of the canonical autophagy machinery. The impact of LAP to immune regulation is best characterized in professional phagocytes, in particular macrophages, where LAP has instrumental roles in the clearance of extracellular particles including apoptotic cells and pathogens. Binding of dead cells via receptors present on the macrophage surface results in the translocation of the autophagy machinery to the phagosome and ultimately LC3 conjugation. These events promote a rapid form of phagocytosis that produces an "immunologically silent" clearance of the apoptotic cells. Consequences of LAP deficiency include a decreased capacity to clear dying cells and the establishment of a lupus-like autoimmune disease in mice. The ability of LAP to attenuate autoimmunity likely occurs through the dampening of pro-inflammatory signals upon engulfment of dying cells and prevention of autoantigen presentation to other immune cells. However, it remains unclear how LAP shapes both the activation and outcome of the immune response at the molecular level. Herein, we provide a detailed review of LAP and its known roles in the immune response and provide further speculation on the putative mechanisms by which LAP may regulate immune function, perhaps through the metabolic reprogramming and polarization of macrophages.

Indexed as

AnimalsHumansInflammationMicrotubule-Associated ProteinsPhagocytosisMAP1LC3A protein, humanMap1lc3b protein, mouseMicrotubule-Associated Proteinsautophagyefferocytosisimmune regulationLC3-associated phagocytosismetabolism

Identifiers

PMID28847720
PMCPMC5743439
OpenAlexW2748829107

What OpenQuestion holds

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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.