Serum IL-10 from systemic lupus erythematosus patients suppresses the differentiation and function of monocyte-derived dendritic cells

被引:17
|
作者
Sun, Zhida [1 ]
Zhang, Rong [2 ]
Wang, Huijuan [3 ]
Jiang, Pengtao [3 ]
Zhang, Jiangquan [3 ]
Zhang, Mingshun [3 ]
Gu, Lei [4 ]
Yang, Xiaofan [3 ]
Zhang, Miaojia [4 ]
Ji, Xiaohui [3 ]
机构
[1] Nanjing Med Univ, Affiliated Stomatol Hosp, Dept Oral Mucosal Dis, Nanjing 210029, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Lab Ctr Basic Med Sci, Nanjing 210029, Jiangsu, Peoples R China
[3] Nanjing Med Univ, Dept Microbiol & Immunol, 140 Hanzhong Rd, Nanjing 210029, Jiangsu, Peoples R China
[4] Nanjing Med Univ, Affiliated Hosp 1, Dept Rheumatol, Nanjing 210029, Jiangsu, Peoples R China
来源
JOURNAL OF BIOMEDICAL RESEARCH | 2012年 / 26卷 / 06期
关键词
lupus erythematosus systemic (SLE); interleukin-10 (IL-10); dendritic cells (DCs); differentiation;
D O I
10.7555/JBR.26.20120115
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The role played by cytokines, other than interferon (IFN)-alpha, in the differentiation and function of dendritic cells (DCs) in systemic lupus erythematosus (SLE), remains unclear. Serum interleukin-10 (IL-10) levels are generally elevated in SLE patients, which might modulate the differentiation of DCs. In this study, DCs were induced from monocytes either by transendothelial trafficking or by culture with granulocyte-macrophage colony-stimulating factor (GM-CSF) + IL-4 + tumor necrosis factor (TNF)-alpha. Both systems were used to investigate the effects of elevated serum IL-10 level on DC differentiation in SLE patients. The results showed that monocyte-derived DCs induced by either SLE serum or exogenous IL-10 reduced the expression of human leukocyte antigen (HLA)-DR and CD80, decreased IL-12p40 level, and increased IL-10 level, and exhibited an impaired capacity to stimulate allogenic T-cell proliferation. These results indicate that serum IL-10 may be involved in the pathogenesis of SLE by modulating the differentiation and function of DCs.
引用
收藏
页码:456 / 466
页数:11
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