The CCL20 and CCR6 axis in psoriasis

• Published in: Scandinavian journal of immunology Vol. 91; no. 3; pp. e12846 - n/a
• Main Authors: Furue, Kazuhisa, Ito, Takamichi, Tsuji, Gaku, Nakahara, Takeshi, Furue, Masutaka
• Format: Journal Article
• Language: English
• Published: England Wiley Subscription Services, Inc 01.03.2020
• Subjects: Animals; Biomarkers; CCL20; CCL20 protein; CCR6; CCR6 protein; Chemokine CCL20 - genetics; Chemokine CCL20 - metabolism; Disease Susceptibility; Effector cells; Gene Expression Regulation - drug effects; Helper cells; Humans; Keratinocytes; Koebner phenomenon; Lymphocytes T; Molecular Targeted Therapy; Psoriasis; Psoriasis - diagnosis; Psoriasis - etiology; Psoriasis - metabolism; Psoriasis - therapy; Receptors, CCR6 - genetics; Receptors, CCR6 - metabolism; Signal Transduction - drug effects; Skin diseases; Th17; Tumor necrosis factor; Koebner phenomenon; CCR6; CCL20; Th17; psoriasis
• ISSN: 0300-9475; 1365-3083; 1365-3083
• DOI: 10.1111/sji.12846

Psoriasis is a TNF‐α/IL‐23/IL‐17A–mediated inflammatory skin disease that causes a significant socioeconomic burden in afflicted patients. IL‐17A–producing immune cells, including Th17 cells, are crucial effector cells in the development of psoriasis. IL‐17A stimulates epidermal keratinocytes to produce CCL20, which eventually recruits CCR6 + Th17 cells into the lesional skin. Thus, the CCL20/CCR6 axis works as a driving force that prepares an IL‐17A–rich cutaneous milieu. In this review, we summarize the current research topics on the CCL20/CCR6 axis and the therapeutic intervention of this axis for psoriasis.