Cytokines IL-17 and IL-22 in the host response to infection
Open accessAbstract
Cytokines IL-17 and IL-22 play pivotal roles in host defense against microbes and in the development of chronic inflammatory diseases. These cytokines are produced by cells that are often located in epithelial barriers, including subsets of T cells and innate lymphoid cells. In general, IL-17 and IL-22 can be characterized as important cytokines in the rapid response to infectious agents, both by recruiting neutrophils and by inducing the production of antimicrobial peptides. Although each cytokine induces an innate immune response in epithelial cells, their functional spectra are generally distinct: IL-17 mainly induces an inflammatory tissue response and is involved in the pathogenesis of several autoimmune diseases, whereas IL-22 is largely protective and regenerative. In this review, we compare IL-17 and IL-22, describing overlaps and differences in their cellular sources as well as their regulation, signaling, biological functions and roles during disease, with a focus on the contribution of these cytokines to the gut mucosal barrier during bacterial infection.
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The presence of all IL-17 and IL-17 receptor paralogs in muskox points to a broad evolutionary conservation of all individual family members in the rapid response to infectious agents.
“pointing to a broad evolutionary conservation of all individual family members in the rapid response to infectious agents112.”
From Chromosomal-level reference genome assembly of muskox (Ovibos moschatus) from Banks Island in the Canadian Arctic, a resource for conservation genomics (2024) · cites this paper as [112]
The section ‘IL-17 and IL-22 are related, but distinct cytokines’ lists the IL-17 and receptor families and says their members share sequence homology. The paper also describes IL-17 responses to infection, but it does not establish evolutionary conservation of every individual family member’s role in a rapid response to infectious agents. (LLM, conf=0.84)
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- Authors
- Valeri, M., & Raffatellu, M.
- Affiliations
- University of California, Irvine (US)
- Corresponding author
- Raffatellu, Manuela
- ORCID
- Raffatellu, Manuela
- Venue
- Pathogens and Disease
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-12
- Volume
- 74
- Issue
- 9
- Pages
- ftw111
- ISSN
- 2049-632X (ISSN-L)
- PMC
- PMC5975231
- OpenAlex
- W2557937803
- Cited by
- 202
- References
- 242
- Citations by year
- 2026: 16 · 2025: 34 · 2024: 22 · 2023: 20 · 2022: 19 · 2021: 29 · 2020: 26 · 2019: 26 · 2018: 4 · 2017: 6
- FWCI
- 1.16
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Pathogens and Disease (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- Burroughs Wellcome Fund
- National Institute of Allergy and Infectious Diseases (R01AI114625, R56AI114625, R21AI121928, R01AI126277, R21AI105374, R37AI126277)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK058057)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- IL-17, IL-22, host defense against infection, innate immunity, epithelial barrier function, gut mucosal barrier, bacterial infection, neutrophil recruitment, antimicrobial peptides, innate lymphoid cells, T cells, cytokine signaling, autoimmune disease, chronic inflammation, tissue regeneration
- MeSH terms
- Interleukin-22, Animals, Enterocolitis, Humans, Infections, Interleukins, Cytokines, Interleukin-17, Host-Pathogen Interactions, Disease Resistance
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