Complement mediated vascular endothelial injury in rheumatoid nodules: a histopathological and immunohistochemical study.
Complement mediated vascular endothelial injury in rheumatoid nodules: a histopathological and immunohistochemical study.
复制标题
类风湿结节中补体介导的血管内皮损伤：组织病理学和免疫组织化学研究。
DOI：
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发表时间：
2000
期刊：
影响因子：
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通讯作者：
T. Ogino
中科院分区：
文献类型：
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作者：
H. Kato;M. Yamakawa;T. Ogino
目标
从形态学和免疫组织化学角度评估 IgM 类风湿因子 (RF) 免疫复合物和补体激活在类风湿结节血管损伤（类风湿关节炎的典型关节外表现）中的作用。
方法
在类风湿结节的小血管中观察到细胞浸润、内皮改变、纤维素样变性和基底膜改变等组织学特征。还进行了免疫组织化学研究。
结果
在一些受损内皮细胞的管腔表面上观察到 IgM RF 和末端补体复合物 (TCC: C5b-9) 的明显共定位。免疫电镜显示内皮囊泡形成，这是针对补体攻击的典型体外保护机制，不仅沉积了 TCC，还沉积了 IgM RF。大多数 TCC 阳性内皮细胞同时表达主要补体调节因子 CD59。
结论
这些数据表明，在类风湿结节中，补体激活介导的血管损伤涉及 IgM RF 在内皮细胞表面的组装。
OBJECTIVE
To evaluate morphologically and immunohistochemically the role of IgM rheumatoid factor (RF) immune complexes and complement activation in rheumatoid nodule vascular injury, a typical extraarticular manifestation of rheumatoid arthritis.
METHODS
Histological features such as cellular infiltration, endothelial alteration, fibrinoid degeneration, and basement membrane alterations were observed in the small vessels in rheumatoid nodules. An immunohistochemical study was also carried out.
RESULTS
Distinct colocalization of IgM RF and terminal complement complexes (TCC: C5b-9) was observed on the luminal surface in some of the damaged endothelial cells. Immuno-electron microscopy revealed endothelial vesiculation, typical of the in vitro protective mechanism against complement attack, with deposition of not only TCC but also IgM RF. Most TCC positive endothelial cells simultaneously expressed the major complement regulatory factor, CD59.
CONCLUSION
These data suggest that, in rheumatoid nodules, vascular injury mediated by complement activation involves the assembly of IgM RF on the endothelial cell surface.