节点1
节点2
发病机制
点头
免疫学
医学
CD80
外周血单个核细胞
肿瘤坏死因子α
CD40
免疫系统
生物
先天免疫系统
细胞毒性T细胞
内分泌学
体外
糖尿病
生物化学
作者
Baoqing Deng,Z. Ye,L. Li,D. Zhang,Yunyun Zhu,Ying He,C. Wang,Lingyan Wu,A. Kijlstra,Peizeng Yang
出处
期刊:Current Molecular Medicine
[Bentham Science]
日期:2016-04-12
卷期号:16 (4): 424-435
被引量:13
标识
DOI:10.2174/1566524016666160316153038
摘要
NOD1 and NOD2 have been found to play a significant regulatory role in autoimmune disease. To analyze the role of NOD1 and NOD2 in the pathogenesis of Vogt- Koyanagi-Harada (VKH) syndrome and Behcet's disease (BD). We analyzed the expression of NOD1 and NOD2 from PBMCs by RT-PCR and Western Blot. PBMCs and DCs were cultured with NOD receptor ligands iE-DAP (NOD1) or MDP (NOD2) and cells and supernatants were analyzed by flow cytometry (FCM) and enzyme-linked immunosorbent assay (ELISA). DCs and CD4+T cells were co-cultured with or without stimulation and cells and supernatants were analyzed by FCM and ELISA. A higher expression of NOD1 and NOD2 was observed in patients with active VKH syndrome as compared with controls. However, no significant differences were found between BD patients and controls. Activation of NOD1 and NOD2 with iE-DAP or MDP markedly increased the level of IL-6, TNF-α and IL-1β in PBMCs and DCs and induced the expression of CD40, CD80, CD83, CD86 and HLA-DR on DCs. Activation of NOD1 and NOD2 in DCs promoted the differentiation and proliferation of CD4T cells. In conclusion, activation of NOD1 or NOD2 increased the production of pro-inflammatory cytokines in PBMCs and promoted the maturation and activation of human DCs in association with stimulation of Th1 and Th17 cells. Our results suggest that over-expression of NOD1 and NOD2 may be involved in the pathogenesis of VKH syndrome. Keywords: NOD-like receptors, dendritic cell, Vogt-Koyanagi-Harada syndrome, Behcet’s disease, uveitis, autoimmune disease.
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