共 234 条
Interleukin-17A and Keratinocytes in Psoriasis
被引:204
作者:

Furue, Masutaka
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Kyushu Univ, Dept Dermatol, Grad Sch Med Sci, Higashi Ku, Maidashi 3-1-1, Fukuoka 8128582, Japan
Kyushu Univ, Res & Clin Ctr Yusho & Dioxin, Higashi Ku, Maidashi 3-1-1, Fukuoka 8128582, Japan
Kyushu Univ, Div Skin Surface Sensing, Grad Sch Med Sci, Higashi Ku, Maidashi 3-1-1, Fukuoka 8128582, Japan Kyushu Univ, Dept Dermatol, Grad Sch Med Sci, Higashi Ku, Maidashi 3-1-1, Fukuoka 8128582, Japan

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

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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
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.
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