Evidence map›Paper›PMID 24586155›Full record

ArticlePLoS pathogens2014

Inflammatory monocytes orchestrate innate antifungal immunity in the lung.

Vanessa Espinosa, Anupam Jhingran, Orchi Dutta, Shinji Kasahara, Robert Donnelly, Peicheng Du, Jeffrey Rosenfeld, Ingrid Leiner, Chiann-Chyi Chen, Yacov Ron and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed
12.9field-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

128 citing papers in PubMed, 174 citations in OpenAlex.

  1. Monocytes in pneumonia: Functional plasticity and innate memory (Review).International journal of molecular medicine · 2026
    Review
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  17. Perforin-2 is dispensable for host defense againstbioRxiv : the preprint server for biology · 2024
    Article
  18. Review
  19. Review
  20. Article

68 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

12 authors at 4 institutions in 1 country.

Vanessa EspinosaRutgers, New Jersey Medical School, Department of Pediatrics, Center for Immunity and Inflammation, Newark, New Jersey, United States of America ; Rutgers, Graduate School of Biomedical Sciences, Newark, New Jersey, United States of America.
Anupam JhingranFred Hutchinson Cancer Research Center, Vaccine and Infectious Disease Division, Seattle, Washington, United States of America.
Orchi DuttaRutgers, New Jersey Medical School, Department of Pediatrics, Center for Immunity and Inflammation, Newark, New Jersey, United States of America ; Rutgers, Graduate School of Biomedical Sciences, Newark, New Jersey, United States of America.
Shinji KasaharaFred Hutchinson Cancer Research Center, Vaccine and Infectious Disease Division, Seattle, Washington, United States of America.
Robert DonnellyRutgers, New Jersey Medical School, Molecular Resource Facility and High Performance and Research Computing Group, Office of Information Technology, Rutgers University, Newark, New Jersey, United States of America.
Peicheng DuRutgers, New Jersey Medical School, Molecular Resource Facility and High Performance and Research Computing Group, Office of Information Technology, Rutgers University, Newark, New Jersey, United States of America.
Jeffrey RosenfeldRutgers, New Jersey Medical School, Molecular Resource Facility and High Performance and Research Computing Group, Office of Information Technology, Rutgers University, Newark, New Jersey, United States of America.
Ingrid LeinerMemorial Sloan Kettering Cancer Center, Sloan Kettering Institute, New York, New York, United States of America.
Chiann-Chyi ChenRutgers, Robert Wood Johnson Medical School, Department of Pharmacology, Piscataway, New Jersey, United States of America.
Yacov RonRutgers, Robert Wood Johnson Medical School, Department of Pharmacology, Piscataway, New Jersey, United States of America.
Tobias M HohlFred Hutchinson Cancer Research Center, Vaccine and Infectious Disease Division, Seattle, Washington, United States of America.
Amariliz RiveraRutgers, New Jersey Medical School, Department of Pediatrics, Center for Immunity and Inflammation, Newark, New Jersey, United States of America.
Rutgers, The State University of New Jersey · USFred Hutch Cancer Center · USRutgers New Jersey Medical SchoolMemorial Sloan Kettering Cancer Center · US

Funding

INITIATION OF THE IMMUNE RESPONSE TO ASPERGILLUS FUMIGATUSR01AI093808 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI HOHL, TOBIAS M · 2011 to 2020
$4.9M
INITIATION OF THE IMMUNE RESPONSE TO ASPERGILLUS FUMIGATUSR37AI093808 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI TOBIAS M HOHL · 2021 to 2026
$4.2M
Dissection of Macrophage Antifungal Activity against Aspergillus fumigatusR21AI105617 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI HOHL, TOBIAS M · 2013 to 2014
$473k
Role of CCR2+ monocytes and Mo-DCs in defense against IA and GVHD developmentR21CA167238 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI RIVERA, AMARILIZ · 2013 to 2014
$375k
CD4+ T cells in Invasive AspergillosisK22CA160874 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI RIVERA, AMARILIZ · 2011 to 2012
$372k
Immune regulatory mechanisms and fungus-specific memory T cell responsesF31AI098408 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ESPINOSA, VANESSA O · 2013 to 2015
$115k
NCI NIH HHS K22 CA160874NCI NIH HHS R21 CA167238NCI NIH HHS R21 CA167238-01A1NIAID NIH HHS F31 AI098408NIAID NIH HHS F31 AI098408-01A1NIAID NIH HHS R01 AI093808NIAID NIH HHS R21 AI105617NIAID NIH HHS R37 AI093808
6 · The paper itself

Abstract

Aspergillus fumigatus is an environmental fungus that causes invasive aspergillosis (IA) in immunocompromised patients. Although -CC-chemokine receptor-2 (CCR2) and Ly6C-expressing inflammatory monocytes (CCR2⁺Mo) and their derivatives initiate adaptive pulmonary immune responses, their role in coordinating innate immune responses in the lung remain poorly defined. Using conditional and antibody-mediated cell ablation strategies, we found that CCR2⁺Mo and monocyte-derived dendritic cells (Mo-DCs) are essential for innate defense against inhaled conidia. By harnessing fluorescent Aspergillus reporter (FLARE) conidia that report fungal cell association and viability in vivo, we identify two mechanisms by which CCR2⁺Mo and Mo-DCs exert innate antifungal activity. First, CCR2⁺Mo and Mo-DCs condition the lung inflammatory milieu to augment neutrophil conidiacidal activity. Second, conidial uptake by CCR2⁺Mo temporally coincided with their differentiation into Mo-DCs, a process that resulted in direct conidial killing. Our findings illustrate both indirect and direct functions for CCR2⁺Mo and their derivatives in innate antifungal immunity in the lung.

Indexed as

AnimalsAspergillus fumigatusCell DifferentiationDendritic CellsDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFlow CytometryImmunity, InnateMiceMice, Inbred C57BLMice, KnockoutMonocytesPulmonary AspergillosisReal-Time Polymerase Chain ReactionReceptors, CCR2Spores, FungalCcr2 protein, mouseReceptors, CCR2

Identifiers

PMID24586155
PMCPMC3930594
OpenAlexW2040810194

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.