Conventional Dendritic Cells Mount a Type I IFN Response against Candida spp. Requiring Novel Phagosomal TLR7-Mediated IFN-β Signaling
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Human fungal pathogens such as the dimorphic Candida albicans or the yeast-like Candida glabrata can cause systemic candidiasis of high mortality in immunocompromised individuals. Innate immune cells such as dendritic cells and macrophages establish the first line of defense against microbial pathogens and largely determine the outcome of infections. Among other cytokines, they produce type I IFNs (IFNs-I), which are important modulators of the host immune response. Whereas an IFN-I response is a hallmark immune response to bacteria and viruses, a function in fungal pathogenesis has remained unknown. In this study, we demonstrate a novel mechanism mediating a strong IFN-β response in mouse conventional dendritic cells challenged by Candida spp., subsequently orchestrating IFN-α/β receptor 1-dependent intracellular STAT1 activation and IFN regulatory factor (IRF) 7 expression. Interestingly, the initial IFN-β release bypasses the TLR 4 and TLR2, the TLR adaptor Toll/IL-1R domain-containing adapter-inducing IFN-β and the β-glucan/phagocytic receptors dectin-1 and CD11b. Notably, Candida-induced IFN-β release is strongly impaired by Src and Syk family kinase inhibitors and strictly requires completion of phagocytosis as well as phagosomal maturation. Strikingly, TLR7, MyD88, and IRF1 are essential for IFN-β signaling. Furthermore, in a mouse model of disseminated candidiasis we show that IFN-I signaling promotes persistence of C. glabrata in the host. Our data uncover for the first time a pivotal role for endosomal TLR7 signaling in fungal pathogen recognition and highlight the importance of IFNs-I in modulating the host immune response to C. glabrata.
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Murine dendritic cells produce IFN-β through the toll-like receptor TLR7, underscoring the role of IFN-I signaling in modulation of the host response to C. glabrata infection.
“Additionally, the murine dendritic cells have also been reported to produce IFN-β through the toll-like receptor TLR7, thereby, underscoring the role of IFN-I signaling in modulation of the host response to C. glabrata infection [146].”
From Candida glabrata: A Lot More Than Meets the Eye (2019) · cites this paper as [146]
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- Authors
- Bourgeois, C., Majer, O., Frohner, I. E., Lesiak-Markowicz, I., Hildering, K.-S., Glaser, W., Stockinger, S., Decker, T., Akira, S., Müller, M., & Kuchler, K.
- Affiliations
- Max Perutz Labs (AT)
- University of Vienna (AT)
- Research Institute for Microbial Diseases, The University of Osaka (JP)
- University of Veterinary Medicine Vienna (AT)
- Corresponding author
- Bourgeois, Christelle
- Majer, Olivia
- Glaser, Walter
- Kuchler, Karl
- ORCID
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-03-01
- Volume
- 186
- Issue
- 5
- Pages
- 3104-3112
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2107406729
- Cited by
- 116
- References
- 63
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 6 · 2023: 4 · 2022: 8 · 2021: 7 · 2020: 9 · 2019: 5 · 2018: 9 · 2017: 6 · 2016: 6 · 2015: 10 · 2014: 12 · 2013: 11 · 2012: 12
- FWCI
- 5.53
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Phaidra (Universität Wien) (submittedVersion, cc-by-nc-nd)
- MPG.PuRe (Max Planck Society) (submittedVersion, other-oa)
- Funders
- Österreichischen Akademie der Wissenschaften
- Bundesministerium für Wissenschaft und Forschung
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Keywords
- myeloid dendritic cells, type I interferon, Candida glabrata, Candida albicans, systemic candidiasis, TLR7, phagosome maturation, phagocytosis, MyD88, IRF1, STAT1, IRF7, fungal pathogen recognition
- MeSH terms
- Animals, Bone Marrow Cells, Candida albicans, Cells, Cultured, Dendritic Cells, Humans, Interferon Type I, Macrophages, Mice, Inbred C57BL, Phagosomes, Signal Transduction, Interferon-beta, Mice, Knockout, Coculture Techniques, Candida glabrata, Toll-Like Receptor 7, Mice
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