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一种用于研究病毒和细胞因子在干燥综合征中作用的模型。

A model to study viral and cytokine involvement in Sjögren's syndrome.

作者信息

Clark D A, Lamey P J, Jarrett R F, Onions D E

机构信息

Department of Veterinary Pathology, Glasgow University Veterinary School, UK.

出版信息

Autoimmunity. 1994;18(1):7-14. doi: 10.3109/08916939409014674.

DOI:10.3109/08916939409014674
PMID:7999958
Abstract

To investigate mechanisms that may be important in the pathogenesis of Sjögren's syndrome (SS) we developed a protocol for the growth of salivary gland epithelial cells in culture. We examined the effect that viral infection has on the cellular location of the autoantigen La. Autoantibodies to La are common in SS and it has been proposed that viral infection may result in cell membrane expression of La. Co-expression of MHC class II molecules in infected cells could lead to the presentation of La peptides to the immune system. Advenovirus infection of salivary gland epithelial cells resulted in an altered nuclear staining of La. Treatment with interferon-gamma resulted in the expression of La in the cell cytoplasm and HLA-DR molecules at the cell surface. These findings suggest that a cytokine-driven mechanism may generate an autoimmune response to La in SS. Using the polymerase chain reaction (PCR) we tested salivary gland epithelial cell cultures for the presence of human herpesvirus-6 (HHV-6) and Epstein-Barr virus (EBV). Only HHV-6 was detected in 2 of 10 salivary gland epithelial cell cultures although the presence of HHV-6 was not associated with SS. Primary salivary gland cultures may prove useful as an in vitro model to study mechanisms of autoimmunity in SS.

摘要

为了研究可能在干燥综合征(SS)发病机制中起重要作用的机制,我们制定了唾液腺上皮细胞体外培养方案。我们研究了病毒感染对自身抗原La细胞定位的影响。抗La自身抗体在SS中很常见,有人提出病毒感染可能导致La在细胞膜上表达。感染细胞中MHC II类分子的共表达可能导致La肽呈递给免疫系统。唾液腺上皮细胞腺病毒感染导致La核染色改变。用γ干扰素处理导致La在细胞质中表达,HLA-DR分子在细胞表面表达。这些发现表明,细胞因子驱动的机制可能在SS中引发针对La的自身免疫反应。我们使用聚合酶链反应(PCR)检测唾液腺上皮细胞培养物中是否存在人疱疹病毒6型(HHV-6)和EB病毒(EBV)。在10个唾液腺上皮细胞培养物中,只有2个检测到HHV-6,尽管HHV-6的存在与SS无关。原代唾液腺培养物可能是研究SS自身免疫机制的有用体外模型。

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