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Interleukin-17A and Keratinocytes in Psoriasis
Masutaka Furue1,2,3, Kazuhisa Furue1, Gaku Tsuji1,2
1Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashiku, Fukuoka 812-8582, Japan.
International Journal of Molecular Sciences
|February 20, 2020
Summary
Interleukin-17A (IL-17A) drives psoriasis by promoting keratinocyte proliferation and inflammation. This review details how IL-17A and skin cells interact to worsen this autoinflammatory skin disease.
Area of Science:
- Immunodermatology
- Molecular biology of skin inflammation
Background:
- Psoriasis is an autoinflammatory skin disease.
- Anti-interleukin 17A (IL-17A) biologics show significant clinical efficacy in treating psoriasis.
- IL-17A plays a critical role in the pathogenesis of psoriasis.
Purpose of the Study:
- To review the interaction between IL-17A and keratinocytes in the context of psoriasis pathogenesis.
- To elucidate the mechanisms by which IL-17A contributes to skin inflammation and characteristic psoriatic lesions.
Main Methods:
- Literature review focusing on IL-17A signaling pathways in keratinocytes.
- Analysis of chemokine and antimicrobial peptide production by keratinocytes.
- Examination of immune cell recruitment mediated by IL-17A-induced factors.
Main Results:
- IL-17A accelerates epidermal keratinocyte proliferation.
- Keratinocytes stimulated by IL-17A produce chemokines (CXCL1, CXCL2, CXCL8, CCL20) and antimicrobial peptides.
- These factors contribute to neutrophil recruitment and the attraction of IL-17A-producing immune cells, creating a pro-inflammatory environment.
Conclusions:
- The IL-17A-keratinocyte axis is a key driver of psoriasis pathogenesis.
- This interaction leads to epidermal hyperplasia, neutrophilic microabscesses, and immune cell infiltration, characteristic of psoriatic skin lesions.
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