Increased expression of human T-cell immunoglobulin- and mucin-domain-containing molecule-4 in peripheral blood mononuclear cells from patients with system lupus erythematosus

Increased expression of human T-cell immunoglobulin- and mucin-domain-containing molecule-4 in peripheral blood mononuclear cells from patients with system lupus erythematosus
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系统性红斑狼疮患者外周血单核细胞中人 T 细胞免疫球蛋白和粘蛋白结构域分子 4 的表达增加

DOI:
10.1038/cmi.2009.118
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发表时间:
2010-02
影响因子:
24.1
通讯作者:
Liang, Xiaohong
Liang, Xiaohong
中科院分区:
医学1区
文献类型:
--
作者:
Zhang, Lining;Liu, Peng;Guo, Chun;Qi, Jianni;Wang, Piming;Xu, Liyun;Ma, Chunhong;Gao, Lifen;Zhao, Peiqing;Liang, Xiaohong

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系统性红斑狼疮(SLE)是一种典型的自身免疫性疾病。固有免疫和适应性免疫共同促进了SLE的发展。抗原呈递细胞(APCs)被认为是连接固有免疫和适应性免疫的纽带。T细胞免疫……
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease. Innate and adaptive immunity cooperatively contribute to the development of SLE. Antigen-presenting cells (APCs) have been suggested to link innate and adaptive immunity. T-cell immunoglobulin- and mucin-domain-containing molecule-4 (Tim-4; also known as Timd4), expressed primarily on the surface of APCs, is a member of the TIM family, a recently described group of molecules that have received much attention as potential regulators of the immune system. In this study, we used quantitative real-time reverse transcription-polymerase chain reaction to examine the mRNA expression of Tim-4 in peripheral blood mononuclear cells (PBMCs) from SLE patients and further analyzed the correlation between the expression of Tim-4 and Tim-1 (a potential ligand for Tim-4) in PBMCs and serum tumor necrosis factor (TNF)-α levels. The results showed that Tim-4 mRNA expression in PBMCs was significantly higher in SLE patients than in healthy controls, especially those patients in the active phase of disease. Moreover, Tim-4 mRNA levels were closely correlated with Tim-1 mRNA levels in PBMCs and with serum TNF-α levels in SLE patients but not in the control group. Taken together, these results demonstrate that Tim-4 may be involved in the pathogenesis of SLE.
系统性红斑狼疮的发病机制
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发表时间: 2009
期刊: --
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