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Updated: Jan 4, 2026
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Lymphocyte Isolation from Human Skin for Phenotypic Analysis and Ex Vivo Cell Culture
Published on: April 8, 2016
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The CCL20 and CCR6 axis in psoriasis.
Kazuhisa Furue1, Takamichi Ito1, Gaku Tsuji2
1Department of Dermatology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.
Scandinavian Journal of Immunology
|November 7, 2019
Summary
Psoriasis involves Tumor Necrosis Factor-alpha (TNF-α), Interleukin-23 (IL-23), and Interleukin-17A (IL-17A). Targeting the CCL20/CCR6 axis offers a promising therapeutic strategy for this inflammatory skin condition.
Area of Science:
- Immunodermatology
- Inflammatory skin diseases
Background:
- Psoriasis is a chronic inflammatory skin condition driven by TNF-α, IL-23, and IL-17A.
- Th17 cells and IL-17A are key players in psoriasis pathogenesis.
- The CCL20/CCR6 axis facilitates the recruitment of immune cells to psoriatic lesions.
Purpose of the Study:
- To review current research on the CCL20/CCR6 axis in psoriasis.
- To explore therapeutic interventions targeting the CCL20/CCR6 pathway.
Main Methods:
- Literature review of studies on psoriasis, IL-17A, CCL20, and CCR6.
- Analysis of the role of the CCL20/CCR6 axis in immune cell trafficking.
- Summary of existing and potential therapeutic strategies.
Main Results:
- The CCL20/CCR6 axis is crucial for recruiting IL-17A-producing Th17 cells to the skin.
- IL-17A induces keratinocytes to produce CCL20, amplifying the inflammatory cycle.
- This axis creates a pro-inflammatory environment conducive to psoriasis development.
Conclusions:
- The CCL20/CCR6 axis is a significant driver of psoriasis.
- Targeting this axis presents a viable therapeutic avenue for managing psoriasis.
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