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目的:建立哮喘特异性免疫治疗小鼠模型,探讨特异性免疫治疗诱导T细胞无能的机制。方法:通过卵蛋白(OVA)皮下注射致敏,雾化吸入激发的方法,建立哮喘特异性免疫治疗的小鼠模型,并通过对肺组织病理切片及支气管肺泡灌洗液(BALF)中的细胞计数及分类,用ELISA法检测血清OVA特异性IgE(sIgE)及脾脏T细胞IL2和IL4的分泌等证实。分离培养脾脏T细胞,用3HTdR掺入法检测其增殖反应;用流式细胞仪(FACS)检测其表面CTLA4分子的表达。结果:与对照组小鼠相比较,哮喘特异性免疫治疗后,小鼠肺组织的炎症病理变化减轻;BALF中嗜酸性粒细胞(EOS)数、血清sIgE的水平、T细胞分泌IL2和IL4的水平以及小鼠对OVA刺激的反应性均显著降低(P<0.01);但T细胞表面CTLA4分子的表达明显上调。结论:建立了哮喘特异性免疫治疗的小鼠模型。T细胞表面CTLA4分子表达的上调可能是哮喘特异性免疫治疗诱导T细胞无能的机制之一。
Objective: To establish a mouse model of asthma-specific immunotherapy to investigate the mechanism of specific immunotherapy-induced T cell incompetence. Methods: A mouse model of asthma-specific immunotherapy was established by subcutaneous injection of ovalbumin (OVA) and sensitized by inhalation by atomization. The lung tissue and the cells in bronchoalveolar lavage fluid (BALF) Count and classify. Serum OVA specific IgE (sIgE) and secretion of IL2 and IL4 in splenic T cells were detected by ELISA. The splenic T cells were isolated and cultured, and the proliferative responses were detected by 3H TdR incorporation. The expression of CTLA4 on the surface of spleen cells was detected by flow cytometry (FACS). Results: Compared with the control group, the inflammatory pathological changes in the lung tissue of mice were relieved after asthma-specific immunotherapy. The levels of eosinophils (EOS) and serum sIgE in BALF, the levels of IL2 and IL4 secreted by T cells (P <0.01). However, the expression of CTLA4 on T cells was significantly up-regulated. Conclusion: A mouse model of asthma-specific immunotherapy was established. Upregulation of CTLA4 molecule expression on T cells may be one of the mechanisms of asthma-specific immunotherapy-induced T cell incompetence.