Interleukin-17A and Keratinocytes in Psoriasis.

Abstract

The excellent clinical efficacy of anti-interleukin 17A (IL-17A) biologics on psoriasis indicates a crucial pathogenic role of IL-17A in this autoinflammatory skin disease. IL-17A accelerates the proliferation of epidermal keratinocytes. Keratinocytes produce a myriad of antimicrobial peptides and chemokines, such as CXCL1, CXCL2, CXCL8, and CCL20. Antimicrobial peptides enhance skin inflammation. IL-17A is capable of upregulating the production of these chemokines and antimicrobial peptides in keratinocytes. CXCL1, CXCL2, and CXCL8 recruit neutrophils and CCL20 chemoattracts IL-17A-producing CCR6+ immune cells, which further contributes to forming an IL-17A-rich milieu. This feed-forward pathogenic process results in characteristic histopathological features, such as epidermal hyperproliferation, intraepidermal neutrophilic microabscess, and dermal CCR6+ cell infiltration. In this review, we focus on IL-17A and keratinocyte interaction regarding psoriasis pathogenesis.

• Authors: Masutaka Furue, Kazuhisa Furue, Gaku Tsuji, Takeshi Nakahara
• Journal: International journal of molecular sciences (Int J Mol Sci) Vol. 21 Issue 4 (Feb 13 2020) ISSN: 1422-0067 [Electronic] Switzerland
• PMID: 32070069 (Publication Type: Journal Article, Review)

Chemical References

• CCL20 protein, human
• CXCL1 protein, human
• CXCL2 protein, human
• CXCL8 protein, human
• Chemokine CCL20
• Chemokine CXCL1
• Chemokine CXCL2
• IL17A protein, human
• Interleukin-17
• Interleukin-8

Topics

• Cell Proliferation (genetics)
• Chemokine CCL20 (genetics)
• Chemokine CXCL1 (genetics)
• Chemokine CXCL2 (genetics)
• Epidermis (metabolism, pathology)
• Humans
• Interleukin-17 (genetics)
• Interleukin-8 (genetics)
• Keratinocytes (metabolism, pathology)
• Neutrophils (metabolism, pathology)
• Psoriasis (genetics, pathology)