Statins inhibit chemotactic interaction between CCL20 and CCR6 in vitro: possible relevance to psoriasis treatment

被引：24

作者：

Kim, Tae-Gyun ^{[1
,2
]}

Byamba, Dashlkhumbe ^{[1
,2
,3
]}

Wu, Wen Hao ^{[1
,2
]}

Lee, Min-Geol ^{[1
,2
,3
]}

机构：

[1] Yonsei Univ, Coll Med, Dept Dermatol, Seoul 120752, South Korea

[2] Yonsei Univ, Coll Med, Cutaneous Biol Res Inst, Seoul 120752, South Korea

[3] Yonsei Univ, Coll Med, Brain Korea Project Med Sci 21, Seoul 120752, South Korea

来源：

EXPERIMENTAL DERMATOLOGY | 2011年 / 20卷 / 10期

关键词：

CCL20; CCR6; IL-23/Th17; axis; psoriasis; statins; CHEMOKINE RECEPTORS; DISEASE; SIMVASTATIN; EXPRESSION; THERAPY; CELLS;

D O I：

10.1111/j.1600-0625.2011.01343.x

中图分类号：

R75 [皮肤病学与性病学];

学科分类号：

100206 ;

摘要：

Psoriasis is a chronic IL-23/Th17 pathway-associated skin disease. An increased expression of lesional CCL20 can recruit CCR6+ Th17, and lesional cytokine milieu persistently activates keratinocytes to produce CCL20. Lipid-lowering drugs, statins, are known to possess immune-modulating functions. In this study, we explored an inhibitory effect of statins on CCL20/CCR6 interaction. We demonstrated that IL-1 beta, TNF-alpha, and IL-17A significantly increased CCL20 production from HaCaT cells. However, these increments were markedly inhibited by fluvastatin and simvastatin, but not by pravastatin. In the chemotaxis migration assay, pretreatment with fluvastatin and simvastatin inhibited the migration of human CD4+ T cells towards CCL20. However, the level of CCR6 surface expression in memory CD4+ T cells was not affected. Our results suggest that not all, but specific types of statins may be of benefit in alleviating psoriasis partially via interrupting CCL20/CCR6 chemotactic interaction, the mechanism which may eventually lessen the infiltration of Th17 cells.

引用

页码：855 / 857

页数：4