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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.

SUBMITTER: Furue M

PROVIDER: S-EPMC7072868 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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Interleukin-17A and Keratinocytes in Psoriasis.

Furue Masutaka M Furue Kazuhisa K Tsuji Gaku G Nakahara Takeshi T

International journal of molecular sciences 20200213 4

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 ...[more]

PMID: 32070069

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Enhanced Migratory Ability of Neutrophils Toward Epidermis Contributes to the Development of Psoriasis <i>via</i> Crosstalk With Keratinocytes by Releasing IL-17A.

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