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器官的非特异性自身免疫性,扩散性红斑狼疮,风湿性多关节炎和Gougeroi—Sjogren综合征的自身免疫性一直被归咎于T淋巴细胞的损伤,B淋巴细胞的逸出和T与B淋巴细胞的共同异常。没有一种假设能概括地阐明所有的临床和实验表现。但是人们强调一些B淋巴细胞能起的作用。它们特异地表达了CD5分子,CD5被单克隆抗体leu-1、OKT1、UCHT2、IOT1、Mid5等识别。然而,起初此标志被认为是T淋巴细胞固有的分子。B-CD5是否存在呢?那是一个进化阶段吗?或是一个独立的系统?它们
The nonspecific autoimmunity of organs, autoimmunity of diffuse lupus erythematosus, rheumatoid polyarthritis and Gougeroi-Sjogren syndrome has been attributed to T lymphocyte injury, B lymphocyte escape and T and B lymphocyte The common exception. No hypothesis can summarize all clinical and experimental findings. But people emphasize that some B lymphocytes can play a role. They express CD5 molecules specifically, and CD5 is recognized by the monoclonal antibodies leu-1, OKT1, UCHT2, IOT1, Mid5 and so on. However, at first this marker was considered as an intrinsic molecule of T lymphocytes. Is B-CD5 present? Is it an evolutionary stage? Or is it an independent system?