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Skeletal Muscle Fibers Express Major Histocompatibility Complex Class II Antigens Independently of Inflammatory Infiltrates in Inflammatory Myopathies

机译:骨骼肌纤维在炎性肌病中独立于炎性浸润物表达主要的组织相容性复合体II类抗原。

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摘要

The aim of our study was to address the question of whether muscle fibers express major histocompatibility complex (MHC) class II in inflammatory myopathies. For this purpose we performed a systematic study of MHC class II antigen expression on muscle fiber membranes in muscle tissue from polymyositis and dermatomyositis patients in various stages of disease activity. Thirty-two patients with classical clinical signs of myositis were divided into subgroups depending on duration of clinical signs of myositis and presence or absence of inflammatory infiltrates in muscle tissue. Immunohistochemistry as well as double-immunofluorescence stainings were used to identify the presence of MHC class II in muscle tissue. MHC class I was included for comparison. Quantification of positive staining was performed using an image analysis system in addition to evaluation by manual microscopic scoring and laser confocal microscopy. It was demonstrated that a significant proportion of skeletal muscle fibers in inflammatory myopathies express MHC class II as well as MHC class I and that MHC antigen expression is independent of the inflammatory cell infiltration. Furthermore, there were no differences in staining pattern between polymyositis and dermatomyositis patients. Our results indicate that MHC class II and MHC class I molecules may be involved in initiating and maintaining the pathological condition in myositis rather than only being a consequence of a preceding local inflammation.
机译:我们研究的目的是解决肌纤维是否在炎症性肌病中表达II类主要组织相容性复合体(MHC)的问题。为此,我们对疾病活动各个阶段的多发性肌炎和皮肌炎患者的肌肉组织中的肌纤维膜上的MHC II类抗原表达进行了系统的研究。根据肌炎的临床体征持续时间和肌肉组织中是否存在炎性浸润,将32例典型的肌炎临床体征患者分为亚组。免疫组织化学和双重免疫荧光染色被用于鉴定肌肉组织中II类MHC的存在。 MHC I类用于比较。除了通过手动显微镜评分和激光共聚焦显微镜进行评估外,还使用图像分析系统对阳性染色进行定量。已经证明,在炎性肌病中大量的骨骼肌纤维表达II类MHC以及I类MHC,并且MHC抗原的表达与炎性细胞浸润无关。此外,多发性肌炎和皮肌炎患者之间的染色方式没有差异。我们的结果表明,MHC II类和MHC I类分子可能参与引发和维持肌炎的病理状况,而不仅仅是先前局部炎症的结果。

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