Evidence map›Paper›PMID 25277143›Full record

ArticleJournal of innate immunity2015

Interferon-γ inhibits nonopsonized phagocytosis of macrophages via an mTORC1-c/EBPβ pathway.

Zengfu Wang, Shuping Zhou, Chenming Sun, Tong Lei, Jianxia Peng, Weiguo Li, Pengbo Ding, Jun Lu, Yong Zhao

Open access · bronzeAbstract read
In one paragraph

Article in Journal of innate immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

22 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. CD4 T Cell-Dependent and -Independent Roles for IFN-γ in Blood-Stage Malaria.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  11. Article
  12. Epithelial sodium channels in macrophage migration and polarization: role of proinflammatory cytokines TNFα and IFNγ.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Frontiers in immunology · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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

9 authors at 2 institutions in 1 country.

Zengfu WangState Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing, PR China.
Shuping Zhou
Chenming Sun
Tong Lei
Jianxia Peng
Weiguo Li
Pengbo Ding
Jun Lu
Yong Zhao
Capital Medical University · CNHenan Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bacterial infection often follows virus infection due to pulmonary interferon-γ (IFN-γ) production during virus infection, which down-regulates macrophage phagocytosis. The molecular mechanisms for this process are still poorly understood. In the present study, IFN-γ treatment significantly inhibited the ability of mouse macrophages to phagocytize nonopsonized chicken red blood cells (cRBCs), bacteria and beads in vitro, while it enhanced IgG- and complement-opsonized phagocytosis. IFN-γ treatment decreased the expression of MARCO (macrophage receptor with collagenous structure) in macrophages. Macrophages showed lower binding to and phagocytic ability of cRBCs when MARCO was blocked with antibody. In addition, IFN-γ induced high activity of mTOR (mammalian target of rapamycin) and decreased the expression of c/EBPβ (CCAAT enhancer-binding protein β) in macrophages. Rapamycin, a specific mTOR inhibitor, significantly reversed the inhibitory effect of IFN-γ on nonopsonized phagocytosis of macrophages and restored c/EBPβ and MARCO expression. Biochemical assays showed that c/EBPβ directly bound to the MARCO gene promoter. Rapamycin significantly hampered the viral-bacterial synergy and protected influenza-infected mice from subsequent bacterial infection. Thus, IFN-γ inhibited the nonopsonized phagocytosis of macrophages through the mTOR-c/EBPβ-MARCO pathway. The present study offered evidence indicating that mTOR may be one of the key target molecules for the prevention of secondary bacterial infection caused by primary virus infection.

Indexed as

AnimalsAntibodies, BlockingCCAAT-Enhancer-Binding Protein-betaChick EmbryoChickensDogsErythrocytesInfluenza A virusInterferon-gammaMacrophagesMadin Darby Canine Kidney CellsMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMultiprotein ComplexesOrthomyxoviridae InfectionsAntibodies, BlockingCCAAT-Enhancer-Binding Protein-betaInterferon-gammaMarco protein, mouseMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesReceptors, ImmunologicTOR Serine-Threonine Kinases

Identifiers

PMID25277143
PMCPMC6738789
OpenAlexW2029630174

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.