Cited by 101Autophagy in Disease and TherapyAntifungal resistance and susceptibilityImmune Response and Inflammation

Dectin-1–Dependent LC3 Recruitment to Phagosomes Enhances Fungicidal Activity in Macrophages

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Tam, Jenny M., Mansour, Michael K., Khan, Nida S., Seward, Michael, Puranam, Sravanthi, Tanne, Antoine, Sokolovska, Anna, Becker, Christine E. +9 more·2014·The Journal of Infectious Diseases

Abstract

Autophagy has been postulated to play role in mammalian host defense against fungal pathogens, although the molecular details remain unclear. Here, we show that primary macrophages deficient in the autophagic factor LC3 demonstrate diminished fungicidal activity but increased cytokine production in response to Candida albicans stimulation. LC3 recruitment to fungal phagosomes requires activation of the fungal pattern receptor dectin-1. LC3 recruitment to the phagosome also requires Syk signaling but is independent of all activity by Toll-like receptors and does not require the presence of the adaptor protein Card9. We further demonstrate that reactive oxygen species generation by NADPH oxidase is required for LC3 recruitment to the fungal phagosome. These observations directly link LC3 to the inflammatory pathway against C. albicans in macrophages.

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Crossref · 10.1093/infdis/jiu290

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  • The role of LAP in immunity against Aspergillus has not been shown for other fungi.

    “Of interest, the role of LAP in immunity against Aspergillus (200, 245) has not been shown for other fungi (255–257).”

    From Aspergillus fumigatus and Aspergillosis in 2019 (2019) · cites this paper as [255]

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Research works printed but not linked: 1

  1. Ma J, Becker C, Lowell CA, Underhill DM. Dectin-1 triggered recruit- ment of LC3 to phagosomes facilitates MHC class II presentation of fungal-derived antigens. J Biol Chem 2012; 41:34149-56.

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Authors
Tam, J. M., Mansour, M. K., Khan, N. S., Seward, M., Puranam, S., Tanne, A., Sokolovska, A., Becker, C. E., Acharya, M., Baird, M. A., Choi, A. M. K., Davidson, M. W., Segal, B. H., Lacy-Hulbert, A., Stuart, L. M., Xavier, R. J., & Vyas, J. M.
Affiliations
  • Harvard University (US)
  • Tisch Cancer Institute (US)
  • Massachusetts General Hospital (US)
  • Broad Institute (US)
  • Benaroya Research Institute (US)
  • Florida State University (US)
  • Weill Cornell Medicine (US)
  • Roswell Park Comprehensive Cancer Center (US)
Corresponding author
Tam, Jenny M.
Venue
The Journal of Infectious Diseases
Published
2014-05-19
Volume
210
Issue
11
Pages
1844-1854
ISSN
  • 0022-1899 (ISSN-L)
  • 1537-6613
OpenAlex
W2069844386
Cited by
101
References
48
Citations by year
2026: 5 · 2025: 5 · 2024: 5 · 2023: 7 · 2022: 6 · 2021: 9 · 2020: 10 · 2019: 14 · 2018: 12 · 2017: 9 · 2016: 12 · 2015: 6 · 2014: 1
FWCI
7.07
Type
journal article
Language
en
Open access
Locations
  • The Journal of Infectious Diseases (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Heart, Lung, and Blood Institute (R01HL055330)
  • National Institute of Allergy and Infectious Diseases (R01AI092084, R01AI097519, R01AI079253)
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
Dectin-1, LC3, autophagy, macrophages, Candida albicans, phagosome, fungal pathogen defense, Syk signaling, NADPH oxidase, reactive oxygen species, cytokine production, CARD9, Toll-like receptors
MeSH terms
Syk Kinase, Dectin-1, Animals, Candida albicans, Cell Line, Fungi, Macrophages, Microtubule-Associated Proteins, Models, Biological, Phagosomes, Phosphorylation, Protein-Tyrosine Kinases, Proteoglycans, Tumor Necrosis Factor-alpha, Signal Transduction, Interleukin-6, Reactive Oxygen Species, NADPH Oxidases, Lectins, C-Type, beta-Glucans, Intracellular Signaling Peptides and Proteins, Mice, CARD Signaling Adaptor Proteins, Interleukin-1beta

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