Cited by 110Psoriasis: Treatment and PathogenesisDermatology and Skin DiseasesSpondyloarthritis Studies and Treatments

Crosstalk: keratinocytes and immune cells in psoriasis

Open access
Kamata, Masahiro, Tada, Yayoi·2023·Frontiers in Immunology

Abstract

In the past, psoriasis was considered a skin disease caused only by keratinocyte disorders. However, the efficacy of immunosuppressive drugs and biologics used to treat psoriasis proves that psoriasis is an immune-mediated disease. Indeed, a variety of immune cells are involved in the pathogenesis of psoriasis, including dendritic cells, Th17 cells, and resident memory T cells. Furthermore, keratinocytes play a role in the development of psoriasis as immune cells by secreting antibacterial peptides, chemokines, tumor necrosis factor-α, interleukin (IL)-36, and IL-23. These immune cells and skin cells interact and drive the aberrant differentiation and proliferation of keratinocytes. This crosstalk between keratinocytes and immune cells critical in the pathogenesis of psoriasis forms an inflammatory loop, resulting in the persistence or exacerbation of psoriasis plaques.

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Crossref · 10.3389/fimmu.2023.1286344

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82 of 82 references verified0 citation errors · 0 not checkable

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  • As psoriatic inflammation persists, lesions become self-sustaining through IL-23 maintaining pathogenic lymphocytes, IL-17 and IL-22 reshaping the epidermis, TNF-α amplifying the inflammatory network, and angiogenic factors such as VEGF remodeling the microvasculature.

    “As this inflammatory process persists, the lesions become self-sustaining: IL-23 maintains pathogenic lymphocytes, IL-17 and IL-22 reshape the epidermis, TNF-α amplifies the inflammatory network, and angiogenic factors such as VEGF remodel the microvasculature.”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [23]

    The sections on pathogenic Th17 cells and TNF-α/IL-36 support IL-23 maintenance of Th17 cells, Th17 cytokine effects on keratinocytes, and a TNF-α-linked inflammatory loop. The Conclusion says this crosstalk maintains psoriasis. Our copy does not support the additional claim that VEGF or other angiogenic factors remodel lesion microvasculature; searches for VEGF and vascular remodeling found no relevant passage. No page numbers are available in the indexed copy. (LLM, conf=0.88)

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  • Keratinocyte activation amplifies the recruitment of neutrophils and additional CCR6+ Th17 cells, reinforcing the inflammatory infiltrate.

    “This keratinocyte activation amplifies the recruitment of neutrophils and additional CCR6+ Th17 cells, reinforcing the inflammatory infiltrate [23,25].”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [23]

    The ‘Chemokines’ section says IL-17-stimulated keratinocytes increase chemokines that likely attract neutrophils and may recruit CCR6+ cells, including Th17 cells. The Conclusion says activated keratinocytes promote further inflammation and inflammatory-cell recruitment. The claim presents the specific recruitment effects as certain, whereas the source qualifies them. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • This mechanistic framework explains the efficacy of biologic therapies targeting TNF, IL-17, and IL-23, which interrupt key nodes in the pathogenic network.

    “This mechanistic framework explains the efficacy of biologic therapies targeting TNF, IL-17, and IL-23, which interrupt key nodes in the pathogenic network.”
  • These cytokines occupy key positions in the dominant pathogenic circuit described in recent psoriasis literature.

    “These cytokines occupy key positions in the dominant pathogenic circuit described in recent psoriasis literature [22,23,24].”
  • Th17-derived cytokines, particularly IL-17A, IL-17F, and IL-22, act directly on keratinocytes, inducing hyperproliferation, impaired terminal differentiation, and increased production of chemokines such as CXCL1, antimicrobial peptides, and pro-inflammatory mediators.

    “Th17-derived cytokines, particularly IL-17A, IL-17F, and IL-22, act directly on keratinocytes, inducing hyperproliferation, impaired terminal differentiation, and a marked increase in the production of chemokines such as CXCL1, antimicrobial peptides, and pro-inflammatory mediators.”

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Authors
Kamata, M., & Tada, Y.
Affiliations
Teikyo University (JP)
Corresponding author
Tada, Yayoi
Venue
Frontiers in Immunology
Published
2023-11-09
Volume
14
Pages
1286344-1286344
ISSN
1664-3224 (ISSN-L)
OpenAlex
W4388615901
Cited by
110
References
82
Citations by year
2026: 50 · 2025: 37 · 2024: 23
FWCI
3.06
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Immunology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Institutional Repositories DataBase (IRDB) (submittedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
  • Health Sciences › Medicine › Rheumatology › Spondyloarthritis Studies and Treatments
Keywords
psoriasis, keratinocytes, immune cells, dendritic cells, Th17 cells, tissue-resident memory T cells, antibacterial peptides, chemokines, TNF-α, IL-36, IL-23, psoriasis pathogenesis, immunosuppressants, biologics
MeSH terms
Humans, Interleukins, Psoriasis, Skin, Tumor Necrosis Factor-alpha, Keratinocytes

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