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目的对严重急性呼吸综合征(SARS)患者脾树突状细胞、巨噬细胞数量和巨噬细胞大小进行定量分析,为SARS的病理变化和发病机制的探讨提供证据。方法通过免疫组织化学技术对6例SARS死亡患者脾和6例意外死亡者正常脾S-100+、CD68+、HLA-DR+、CD83+细胞的分布进行观察,并采用图像分析系统对阳性细胞数量或体积进行分析。结果SARS死亡患者脾内白髓中S-100+树突状细胞数较正常平均减少80.49%,有的甚至完全消失;脾红髓中CD68+巨噬细胞数量较正常平均减少39.48%,体积是正常平均值的2.21倍。脾白髓中HLA-DR+抗原呈递细胞明显减少。SARS死亡患者脾与正常脾中均无CD83+成熟树突状细胞。结论SARS患者免疫系统中抗原呈递系统遭到严重破坏,支持SARS是一种病毒性免疫缺陷病。SARS病毒不能引发树突状细胞成熟。巨噬细胞的体积增大处于激活状态,提示巨噬细胞在SARS发病机制中起一定作用。
Objective To quantitatively analyze the splenic dendritic cells, the number of macrophages and the size of macrophages in patients with severe acute respiratory syndrome (SARS), so as to provide evidences for the pathological changes and pathogenesis of SARS. Methods The distribution of S-100 +, CD68 +, HLA-DR + and CD83 + cells in spleen and 6 cases of accidental death in 6 SARS patients were detected by immunohistochemistry. The number of positive cells or volume Analyze. Results The number of S-100 + dendritic cells in spleen white matter of SARS patients was 80.49% less than normal, and some even completely disappeared. The number of CD68 + macrophages in spleen red blood cells was reduced by 39.48% compared with normal, the volume was normal 2.21 times the average. HLA-DR + antigen-presenting cells in spleen and white marrow were significantly reduced. There was no CD83 + mature dendritic cells in spleen and normal spleen of SARS patients. Conclusion The antigen presenting system in the immune system of SARS patients has been severely damaged, supporting that SARS is a viral immunodeficiency disease. SARS virus can not trigger dendritic cell maturation. The enlargement of macrophages is activated, suggesting that macrophages play a role in the pathogenesis of SARS.