20立方厘米
C-C趋化因子受体6型
趋化因子
强直性脊柱炎
炎症
医学
免疫学
外周血单个核细胞
药理学
趋化因子受体
生物
体外
生物化学
作者
Eun Jeong Won,Hui-Ju Kim,Yu Jeong Lee,Moon‐Ju Kim,Hae-In Lee,Hyun Hee Jang,Seong Hoon Kim,Ji‐Hyoun Kang,Ki‐Jeong Park,Seung Cheol Shim,Sungsin Jo,So Yeon Kim,Tae‐Jong Kim
出处
期刊:Rheumatology
[Oxford University Press]
日期:2023-06-05
卷期号:62 (12): 4000-4005
标识
DOI:10.1093/rheumatology/kead268
摘要
Abstract Objectives Th17 cells are known to play a significant role in AS. C-C motif chemokine ligand 20 (CCL20) binds to C-C chemokine receptor 6 (CCR6) on Th17 cells, promoting their migration to inflammation sites. The aim of this research is to examine the effectiveness of CCL20 inhibition in treating inflammation in AS. Methods Mononuclear cells from peripheral blood (PBMC) and SF (SFMC) were collected from healthy individuals and AS. Flow cytometry was used to analyse cells producing inflammatory cytokines. CCL20 levels were determined using ELISA. The impact of CCL20 on Th17 cell migration was verified using a Trans-well migration assay. The in vivo efficacy of CCL20 inhibition was evaluated using an SKG mouse model. Results The presence of Th17 cells and CCL20 expressing cells was higher in SFMCs from AS patients compared with their PBMCs. The CCL20 level in AS SF was significantly higher than in OA patients. The percentage of Th17 cells in PBMCs from AS patients increased when exposed to CCL20, whereas the percentage of Th17 cells in SFMCs from AS patients decreased when treated with CCL20 inhibitor. The migration of Th17 cells was found to be influenced by CCL20, and this effect was counteracted by the CCL20 inhibitor. In the SKG mouse model, the use of CCL20 inhibitor significantly reduced joint inflammation. Conclusion This research validates the critical role of CCL20 in AS and suggests that targeting CCL20 inhibition could serve as a novel therapeutic approach for AS treatment.
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