Evidence map›Paper›PMID 26965632›Full record

ArticleJournal of leukocyte biology2016

PKC-δ activation in neutrophils promotes fungal clearance.

Xun Li, Xavier Cullere, Hiroshi Nishi, Gurpanna Saggu, Enrique Durand, Michael K Mansour, Jenny M Tam, Xiu-Yu Song, Xin Lin, Jatin M Vyas and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

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  9. It takes a village: Phagocytes play a central role in fungal immunity.Seminars in cell & developmental biology · 2019
    Review
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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

11 authors at 5 institutions in 2 countries.

Xun LiCenter for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA; Department of Laboratory Medicine, The First Affiliated Hospital, Medical College of Xiamen University, Xiamen, Fujian, China;
Xavier CullereCenter for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA;
Hiroshi NishiCenter for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA;
Gurpanna SagguCenter for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA;
Enrique DurandCenter for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA;
Michael K MansourDepartment of Medicine, Division of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA; and.
Jenny M TamDepartment of Medicine, Division of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA; and.
Xiu-Yu SongDepartment of Laboratory Medicine, The First Affiliated Hospital, Medical College of Xiamen University, Xiamen, Fujian, China;
Xin LinDepartment of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Jatin M VyasDepartment of Medicine, Division of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA; and.
Tanya MayadasCenter for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA; tmayadas@rics.bwh.harvard.edu.
Harvard University · USBrigham and Women's Hospital · USMassachusetts General Hospital · USFirst Affiliated Hospital of Xiamen University · CNThe University of Texas MD Anderson Cancer Center · US

Funding

INFECTIOUS DISEASE AND BASIC MICROBIOLOGICAL MECHANISMST32AI007061 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI Marcia B Goldberg · 1985 to 2026
$12.1M
Regulators of Immune Complex Mediated Neutrophil Recruitment and Tissue InjuryR01HL065095 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI MAYADAS, TANYA N · 1999 to 2025
$11.9M
Functional Role of the Tetraspanin CD82/Kai1 in Innate and Adaptive ImmunityR01AI092084 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI VYAS, JATIN M · 2011 to 2015
$2.2M
Negative regulation of C-type lectin receptor signaling in response to fungal infectionR01AI116722 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI YING, HAOQIANG · 2016 to 2020
$2.0M
The role of TLR9 on Aspergillus fumigatus phagosomesR01AI097519 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI VYAS, JATIN M · 2013 to 2016
$1.6M
Subcellular Mechanisms for Fungal Phagosome Maturation in MacrophagesK08AI110655 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI MANSOUR, MICHAEL K · 2014 to 2017
$759k
Mechanism of host innate immune system sensing Candida albicans infectionR56AI050848 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LIN, XIN · 2014 to 2014
$305k
NHLBI NIH HHS R01 HL065095NIAID NIH HHS K08 AI110655NIAID NIH HHS R01 AI092084NIAID NIH HHS R01 AI097519NIAID NIH HHS R01 AI116722NIAID NIH HHS R56 AI050848NIAID NIH HHS T32 AI007061
6 · The paper itself

Abstract

The C-type lectin receptor dectin-1 and the integrin Mac-1 have key roles in controlling fungal infection. Here, we demonstrate that dectin-1- and Mac-1-induced activation of protein kinase Cδ in neutrophils, independent of the Card9 adaptor, is required for reactive oxygen species production and for intracellular killing upon Candida albicans uptake. Protein kinase Cδ was also required for zymosan-induced cytokine generation in neutrophils. In macrophages, protein kinase Cδ deficiency prevented fungi-induced reactive oxygen species generation but had no effect on activation of TGF-β-activated kinase-1, an effector of Card9, or nuclear factor κB activation, nor did it affect phagolysosomal maturation, autophagy, or intracellular C. albicans killing. In vivo, protein kinase Cδ-deficient mice were highly susceptible to C. albicans and Aspergillus fumigatus infection, which was partially rescued with adoptively transferred wild-type neutrophils. Thus, protein kinase Cδ activation downstream of dectin-1 and Mac-1 has an important role in neutrophil, but not macrophage, functions required for host defense against fungal pathogens.

Indexed as

AnimalsAspergillosisAspergillus fumigatusCandida albicansCandidiasisCARD Signaling Adaptor ProteinsCytokinesDectin-1FemaleLectins, C-TypeMacrophage-1 AntigenMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutCard9 protein, mouseCARD Signaling Adaptor ProteinsCytokinesDectin-1Lectins, C-TypeMacrophage-1 AntigenNF-kappa BPrkcd protein, mouseProtein Kinase C-deltaReactive Oxygen SpeciesTransforming Growth Factor betaC. albicansdectin-1host defenseMac-1reactive oxygen speciessignaling

Identifiers

PMID26965632
PMCPMC6608027
OpenAlexW2296195425

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.