The Roles of Type I Interferon in Bacterial Infection
Open accessAbstract
Type I interferons (IFNs) are pleiotropic cytokines well recognized for their role in the induction of a potent antiviral gene program essential for host defense against viruses. They also modulate innate and adaptive immune responses. However, the role of type I IFNs in host defense against bacterial infections is enigmatic. Depending on the bacterium, they exert seemingly opposite and capricious functions. In this review, we summarize the effect of type I IFNs on specific bacterial infections and highlight the effector mechanisms regulated by type I IFNs in an attempt to elucidate new avenues to understanding their role.
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The TII response is also induced by bacterial, parasitic, and fungal infections.
“this response is also induced by bacterial, parasitic (43), and fungal infections (30, 44 – 48).”
From Overlooked <i>Candida glabrata</i> petites are echinocandin tolerant, induce host inflammatory responses, and display poor <i>in vivo</i> fitness (2023) · cites this paper as [43]
The “Pathways of recognition and response” section states that bacterial components induce type I interferons, supporting the bacterial part of the claim. Our copy does not establish that parasitic or fungal infections induce this response; searches for those infections found no relevant passage. No page numbers are available in the indexed copy. (LLM, conf=0.87)
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Flagged first, then by citations
Cited by
Sorted by citations
Mouse model of SARS-CoV-2 reveals inflammatory role of type I interferon signaling
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“Although classically associated with viral infection, this response is also induced by bacterial, parasitic (43), and fungal infections (30, 44–48).”
BackgroundRiedelberger, M., Penninger, P., Tscherner, M., Hadriga, B., Brunnhofer, C., Jenull, S., Stoiber, A., Bourgeois, C., Petryshyn, A., Glaser, W., et al. (2020) · iScience · doi:10.1016/j.isci.2020.101121 · Cited by 23 · see citing works
- Authors
- Boxx, G. M., & Cheng, G.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Cheng, Genhong
- Venue
- Cell Host & Microbe
- Publisher
- Elsevier BV
- Published
- 2016-06
- Volume
- 19
- Issue
- 6
- Pages
- 760-769
- ISSN
- 1931-3128 (ISSN-L)
- PMC
- PMC5847370
- OpenAlex
- W2418688677
- Cited by
- 335
- References
- 100
- Citations by year
- 2026: 24 · 2025: 36 · 2024: 38 · 2023: 39 · 2022: 38 · 2021: 46 · 2020: 45 · 2019: 32 · 2018: 19 · 2017: 13 · 2016: 5
- FWCI
- 2.19
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Host & Microbe (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (R01AI069120, R01AI056154, R01AI078389)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Microbiology › Antimicrobial Peptides and Activities
- Keywords
- type I interferon, bacterial infection, host defense, innate immunity, effector mechanisms, host-pathogen interaction
- MeSH terms
- Animals, Anti-Inflammatory Agents, Bacterial Infections, Humans, Immunity, Innate, Interferon Type I, Interferon-gamma, Signal Transduction, Cytokines, Antimicrobial Cationic Peptides, Adaptive Immunity
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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