论文部分内容阅读
随着H IV感染者及各类医疗措施导致的免疫受损者的增多,探讨一种适合免疫缺陷人群的预防机会感染的策略越来越受到重视。研究表明,CD4+T细胞是抵抗肺孢子菌等机会感染的最主要因素,但不是唯一的因素。其中CD40配体(CD40L)被认为是一种可以启动B细胞和CD8+T细胞反应的关键因子。为探讨CD40L是否能在缺乏CD4+T细胞的小鼠体内启动免疫反应,本文研究了用卵白蛋白(OVA)作为模型抗原,联合应用CD40L引起的免疫反应。结果显示,同时应用OVA和CD40L,可使CD4+T细胞耗竭小鼠体内抗OVA IgG抗体和抗原特异性IFN明显增多,提示在CD4+T细胞缺乏的宿主体内,CD40L可以启动B细胞和CD8+T细胞类免疫反应。该结果为抗肺孢子菌等机会性感染的免疫预防研究提供可贵的资料。
With the increasing number of immunocompromised patients with H IV infection and various medical measures, it is more and more important to explore a strategy to prevent opportunistic infections in a population suitable for immunodeficiency. Studies have shown that, CD4 + T cells are the most important factor in resistance to opportunistic infections such as Pneumocystis, but not the only factor. Among them, CD40 ligand (CD40L) is considered to be a key factor that can initiate B cell and CD8 + T cell response. In order to investigate whether CD40L can initiate an immune response in mice lacking CD4 + T cells, this study investigated the immunological response to ovalbumin (OVA) as a model antigen in combination with CD40L. The results showed that simultaneous application of OVA and CD40L can make CD4 + T cells depleted mice anti-OVA IgG antibody and antigen-specific IFN significantly increased, suggesting that in CD4 + T cell deficient host, CD40L can activate B cells and CD8 + T cell immune response. The results provide valuable information for immunoprecipitation research on opportunistic infections such as Pneumocystis sp.