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LMP-1、FAS及FAS-L在组织细胞坏死性淋巴结炎中的表达 被引量:2

EXPRESSION OF LMP-1, FAS AND FAS-L IN HISTIOCYTIC NECROTIZING LYMPHADENITIS
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摘要 ①目的探讨EB病毒、FAS及FASL在组织细胞坏死性淋巴结炎病因及发病机制中所起的作用及相互关系。②方法应用免疫组化SP法对40例组织细胞坏死性淋巴结炎和10例反应性增生淋巴结组织中的EB病毒潜伏膜蛋白(LMP1)、FAS及FASL蛋白的表达进行检测。③结果LMP1、FAS、FASL在组织细胞坏死性淋巴结炎的表达均比对照组明显增高(χ2=4.188,P<0.05)。LMP1的表达与FAS及FASL呈正相关(χ2=4.365、4.000,P<0.05)。④结论EB病毒是组织细胞坏死性淋巴结炎的发病原因之一,FAS与FASL介导的细胞毒性反应为引起EB病毒感染淋巴细胞凋亡的主要原因之一。 Objective To study the function of and relationship between EB virus, FAS and FAS-L in the pathogenesis of histiocytic necrotizing lymphadenitis. Methods The expressions of LMP-1, FAS and FAS-L in specimens of 40 cases of histiocytic necrotizing lymphadenitis and 10 cases of reactive hyperplastic lymphadenopathy were detected by S-P immunohistochemical staining. Results The positive expressions of LMP-1,FAS and FAS-L were obviously higher than the control (x^2 =4. 188,P〈0. 05). There was positive relationship between the expressions of LMP-1 and FAS/FA-L (x^2=4. 365,4. 000;P〈0.05). Conclusion Pathogenesis of necrotizing lymphadenitis is related to EB virus. FAS-based and T-cell-mediated cytotoxicity was the main reason of the apoptosis of EBV infected cells in histiocytic necrotizing lymphadenitis.
出处 《齐鲁医学杂志》 2005年第3期209-210,共2页 Medical Journal of Qilu
关键词 组织细胞坏死性淋巴结炎 疱疹病毒4型 FAS FAS-L 免疫组织化学 histiocytic necrotizing lymphadenitis herpesvirus 4, human FAS FAS-L immunohistochemistry
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  • 2Ohshima K, Shimazaki K, Kume T, et al. Perforin and Fas pathways of cytotoxic T-cells in histioctic necrotizing lymphadenitis[J]. Histopathology, 1998, 33:471.
  • 3Chiu CF, Chow KC, Lin TY, et al. Virus infection in patients with histoeytie neerotizing lymphadenitis in Taiwan: detection of Epstein-Barr Virus, type I human T-cell lymphotropic virus, and parvovirus B19[J]. Am J Clin Pathol, 2000, 113 :774.
  • 4Felgar RE, Furth EE, Wasih MA, et al. Histocytic necrotizing lymphadenitis (Kikuchi's disease) : in situ end-labeling,immunohistochemical and serologhic evidence supporting cytotoxic lymphocyte-mediated apoptotic cell death [J]. Med Pathol, 1997, 10: 231.

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