Cited by 864Psoriasis: Treatment and PathogenesisCytokine Signaling Pathways and InteractionsDermatology and Skin Diseases

IL-22 Inhibits Epidermal Differentiation and Induces Proinflammatory Gene Expression and Migration of Human Keratinocytes

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Boniface, Katia, Bernard, François-Xavier, Garcia, Martine, Gurney, Austin L, Lecron, Jean-Claude, Morel, Franck·2005·The Journal of Immunology

Abstract

IL-22 belongs to a family of cytokines structurally related to IL-10, including IL-19, IL-20, IL-24, and IL-26. In contrast to IL-10, IL-22 has proinflammatory activities. IL-22 signals through a class II cytokine receptor composed of an IL-22-binding chain, IL-22RA1, and the IL-10RB subunit, which is shared with the IL-10R. In the present study, we show that short-term cultured human epidermal keratinocytes express a functional IL-22R but no IL-10R. Accordingly, IL-22 but not IL-10 induces STAT3 activation in keratinocytes. Using a cDNA array screening approach, real-time RT-PCR, and Western blot analysis, we demonstrate that IL-22 up-regulates, in a dose-dependent manner, the expression of S100A7, S100A8, S100A9, a group of proinflammatory molecules belonging to the S100 family of calcium-binding proteins, as well as the matrix metalloproteinase 3, the platelet-derived growth factor A, and the CXCL5 chemokine. In addition, IL-22 induces keratinocyte migration in an in vitro injury model and down-regulates the expression of at least seven genes associated with keratinocyte differentiation. Finally, we show that IL-22 strongly induces hyperplasia of reconstituted human epidermis. Taken together, these results suggest that IL-22 plays an important role in skin inflammatory processes and wound healing.

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  • In vitro studies suggest that IL-22 signals to epithelial keratinocytes of the skin to promote proliferation and migration and induce AMPs.

    “In vitro studies have suggested that IL-22 signals to epithelial keratinocytes of the skin to promote proliferation and migration and inducing AMPs.85,86”

    From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [85]

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Authors
Boniface, K., Bernard, F.-X., Garcia, M., Gurney, A. L., Lecron, J.-C., & Morel, F.
Affiliations
  • Université de Poitiers (FR)
  • BIOalternatives , Gençay ,
  • Genentech (US)
Venue
The Journal of Immunology
Published
2005-03
Volume
174
Issue
6
Pages
3695-3702
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
OpenAlex
W1576903429
Cited by
864
References
54
Citations by year
2026: 10 · 2025: 31 · 2024: 36 · 2023: 35 · 2022: 46 · 2021: 55 · 2020: 35 · 2019: 34 · 2018: 38 · 2017: 56 · 2016: 45 · 2015: 55 · 2014: 48 · 2013: 56 · 2012: 73
FWCI
9.10
Type
journal article
Language
en
Open access
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Funders
Centre Hospitalier Universitaire de Poitiers
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
Keywords
IL-22, keratinocytes, epidermal differentiation, keratinocyte migration, STAT3 activation, IL-22 receptor, IL-10 receptor, S-100 protein, matrix metalloproteinase-3, PDGF-A, CXCL5, skin inflammation, wound healing, epidermal hyperplasia
MeSH terms
S100 Calcium Binding Protein A7, Interleukin-22, Base Sequence, Calcium-Binding Proteins, Cell Differentiation, Cell Movement, Cells, Cultured, DNA, DNA-Binding Proteins, Humans, Interleukins, S100 Proteins, Recombinant Proteins, RNA, Messenger, Signal Transduction, Trans-Activators, Keratinocytes, Gene Expression, Interleukin-10, Receptors, Interleukin, Inflammation Mediators, Matrix Metalloproteinase 3, Oligonucleotide Array Sequence Analysis, Calgranulin A, Calgranulin B, STAT3 Transcription Factor

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