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我们从一例并发单纯性红细胞再生障碍性贫血(纯红再障)和一例并发重症肌无力的胸腺癌患者获得胸腺癌组织内的胸腺细胞和外周血单个核细胞等。利用流式细胞仪对这些细胞的表型进行了分析,结果表明胸腺细胞呈现过度成熟状态,并发纯红再障患者的胸腺瘤中的胸腺细胞,外周血及骨髓中的单个核细胞三种细胞群体的共同特征是CD8~+T细胞比正常人显著增加。而并发重症肌无力患者的胸腺癌组织中胸腺细胞以CD4~+8~-细胞占优势,而CD4~-8~+细胞很少,成熟型和早期胸腺细胞均较正常胸腺增加,而处于中间发育阶段的胸腺细胞显著减少。其外周血中T细胞亚群组成则无明显改变。根据这些结果,我们提出胸腺癌并发纯红再障的发病机理。即:特定型别胸腺上皮细胞发生肿瘤,肿瘤性上皮细胞诱导CD8~+T细胞优势分化并进入外周血和骨髓,进而直接抑制或通过淋巴因子间接抑制红细胞的生成,从而导致纯红再障。而胸腺瘤并发重症肌无力的发病机理则不同于纯红再障,我们认为并发重症肌无力的原因在于胸腺癌组织本身。瘤细胞产生的某种细胞因子导致了重症肌无力的发生。或者是瘤组织所输出的CD4~+8~-T细胞较少,并未影响T细胞亚群的改变,但是功能发生异常,从而打破了B细胞的自身耐受,进而产生抗乙酰胆碱受体的自身抗体。而自身抗体才是重症肌无?
We obtained thymocytes and peripheral blood mononuclear cells from thymoma tissues from one patient with thymoma complicated with simple red cell aplasia (pure red aplasia) and one with myasthenia gravis. The phenotypes of these cells were analyzed by flow cytometry and the results showed that the thymocytes presented an over-mature state with thymocytes in thymoma, peripheral blood and mononuclear cells in the bone marrow of patients with pure red aromatherapy The common feature of the population is that CD8 + T cells are significantly increased compared to normal individuals. Thymic cells in thymus tissue of patients with myasthenia gravis dominated CD4 ~ + 8 ~ - cells, while CD4 ~ -8 ~ + cells were rare, while mature and early thymocytes increased compared with normal thymus, while in the middle Thymus cells at developmental stages are significantly reduced. T lymphocyte subsets in peripheral blood composition did not change significantly. Based on these results, we propose the pathogenesis of pure red aplastic anemia in thymoma. That is: specific types of thymic epithelial tumor, tumor epithelial cells induced differentiation of CD8 ~ T cells and enter the peripheral blood and bone marrow, and then directly or indirectly through inhibition of lymphokine production of red blood cells, resulting in pure red aplastic anemia. The pathogenesis of thymoma complicated with myasthenia gravis is different from pure red aplasia, we believe that the cause of myasthenia gravis complicated by thymoma tissue itself. Certain cytokines produced by tumor cells lead to the development of myasthenia gravis. Or tumor tissue output of CD4 ~ +8 ~ -T cells less, did not affect the T cell subsets change, but the function abnormalities, which broke the B cell self-tolerance, and then produce anti-acetylcholine receptor Autoantibodies. The autoantibody is myasthenia gravis?