Interleukin-17A and Keratinocytes in Psoriasis

被引：209

作者：

Furue, Masutaka ^{[1
,2
,3
]}

Furue, Kazuhisa ^{[1
]}

Tsuji, Gaku ^{[1
,2
]}

Nakahara, Takeshi ^{[1
,3
]}

机构：

[1] Kyushu Univ, Dept Dermatol, Grad Sch Med Sci, Higashi Ku, Maidashi 3-1-1, Fukuoka 8128582, Japan

[2] Kyushu Univ, Res & Clin Ctr Yusho & Dioxin, Higashi Ku, Maidashi 3-1-1, Fukuoka 8128582, Japan

[3] Kyushu Univ, Div Skin Surface Sensing, Grad Sch Med Sci, Higashi Ku, Maidashi 3-1-1, Fukuoka 8128582, Japan

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2020年 / 21卷 / 04期

关键词：

psoriasis; keratinocytes; interleukin-17A; Th17; ILC3; CCL20; CXCL1; CXCL8; Koebner phenomenon; antimicrobial peptides; GROWTH-FACTOR RECEPTOR; INNATE LYMPHOID-CELLS; DELTA T-CELLS; IN-VIVO IMPLICATIONS; KAPPA-B-ZETA; ATOPIC-DERMATITIS; JAPANESE PATIENTS; PLAQUE PSORIASIS; ANTIMICROBIAL PEPTIDES; DENDRITIC CELLS;

D O I：

10.3390/ijms21041275

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页数：21

共 234 条

[1] Epidermal growth factor receptor signalling regulates granulocyte-macrophage colony-stimulating factor production by airway epithelial cells and established allergic airway disease [J].