IL-22 promotes fibroblast-mediated wound repair in the skin
Open accessAbstract
Skin wound repair requires complex and highly coordinated interactions between keratinocytes, fibroblasts, and immune cells to restore the epidermal barrier and tissue architecture after acute injury. The cytokine IL-22 mediates unidirectional signaling from immune cells to epithelial cells during injury of peripheral tissues such as the liver and colon, where IL-22 causes epithelial cells to produce antibacterial proteins, express mucins, and enhance epithelial regeneration. In this study, we used IL-22(-/-) mice to investigate the in vivo role for IL-22 in acute skin wounding. We found that IL-22(-/-) mice displayed major defects in the skin's dermal compartment after full-thickness wounding. We also found that IL-22 signaling is active in fibroblasts, using in vitro assays with primary fibroblasts, and that IL-22 directs extracellular matrix (ECM) gene expression and myofibroblast differentiation both in vitro and in vivo. These data define roles of IL-22 beyond epithelial cross talk, and suggest that IL-22 has a previously unidentified role in skin repair by mediating interactions between immune cells and fibroblasts.
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IL-22 has a similar effect to IL-4 and IL-13.
“IL-22 has been described to have similar effect (118).”
From Unraveling SSc Pathophysiology; The Myofibroblast (2018) · cites this paper as [118]
Th17 cells can play a role in fibrosis, in part via their production of IL-17 and IL-22, which can stimulate collagen, TGFβ, and IL-6 production in pulmonary fibroblasts.
“Also T helper 17 cells (Th17) can play a role in fibrosis, in part via their production of IL-17 and IL-22, which can stimulate collagen, TGFβ and IL-6 production in pulmonary fibroblasts (117, 118).”
From Unraveling SSc Pathophysiology; The Myofibroblast (2018) · cites this paper as [118]
IL-22 has an essential role in the wound healing response, demonstrated in IL-22−/− mice.
“An essential role for IL-22 in the wound healing response has been demonstrated in IL-22−/− mice.”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [87]
The delayed wound healing response in IL-22−/− mice is attributed to defective fibronectin and collagen production by fibroblasts and impaired myofibroblast differentiation rather than to keratinocyte-mediated effects.
“The delayed wound healing response in IL-22−/− mice has been attributed to defective fibronectin and collagen production by fibroblasts and impaired myofibroblast differentiation rather than to keratinocyte-mediated effects.87”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [87]
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References 59 · Cited by 161
- Authors
- McGee, H. M., Schmidt, B. A., Booth, C. J., Yancopoulos, G. D., Valenzuela, D. M., Murphy, A. J., Stevens, S., Flavell, R. A., & Horsley, V.
- Affiliations
- Howard Hughes Medical Institute (US)
- Yale University (US)
- Regeneron (United States) (US)
- Corresponding author
- Flavell, Richard A.
- Horsley, Valerie
- ORCID
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2013-05
- Volume
- 133
- Issue
- 5
- Pages
- 1321-1329
- ISSN
- 0022-202X (ISSN-L)
- PMC
- PMC3610794
- OpenAlex
- W2115510769
- Cited by
- 161
- References
- 59
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 17 · 2023: 12 · 2022: 15 · 2021: 11 · 2020: 11 · 2019: 13 · 2018: 19 · 2017: 14 · 2016: 14 · 2015: 9 · 2014: 9 · 2013: 5
- FWCI
- 7.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- Yale University
- National Institutes of Health
- National Institute of General Medical Sciences (T32-GM07205, T32GM007223, T32GM007205)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR060295)
- Topics
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- IL-22, skin wound healing, fibroblasts, myofibroblast differentiation, extracellular matrix gene expression, keratinocytes
- MeSH terms
- Interleukin-22, Animals, Cell Differentiation, Cells, Cultured, Extracellular Matrix, Fibroblasts, Interleukins, Male, RNA, Messenger, Skin, Wound Healing, Signal Transduction, Mice, Knockout, Models, Animal, Mice, Myofibroblasts
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