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目的:研究小鼠模型中天花粉蛋白(TCS)诱导的卵清白蛋白(OVA)特异性的E型免疫球蛋白(IgE)应答反应的可能机理。方法:首先用抗白介素-4(IL-4)的单抗治疗TCS和卵清白蛋白(OVA)免疫的小鼠,通过减少内源性IL-4的水平,以观察其对血清中IgE抗体水平的影响。其次,用重组IL-4处理小鼠,通过增加外源性IL-4的水平观察其对血清中OVA特异性IgE形成的影响。最后,我们在TCS免疫小鼠IgE形成过程中,用半定量PCR方法检测了腹腔淋巴结中CD40的配体(CD40L),肿瘤坏死因子-α(TNF-α)和白介素-13(IL-13)基因表达的趋势。结果:抗IL-4的单抗可以抑制TCS对OVA诱导的特异性IgE的形成,但重组IL-4本身并不能引起OVA特异的IgE应答反应。在TCS的初次和二次免疫中均有较高的表达峰,且CD40L的表达峰与IL-4类似,仅持续较短的时间。结论:IL-4对于TCS诱导的IgE应答反应为必要非充分条件。CD40L、TNF-α和IL-13可能也参与了此过程,其中CD40L可能具有与IL-4同样重要的作用。
AIM: To investigate the possible mechanism of TCS-induced ovalbumin (OVA) -specific immunoglobulin (IgE) response in mouse models. Methods: First, mice immunized with TCS and OVA were treated with anti-IL-4 mAb to reduce the level of endogenous IL-4 and to observe their effect on serum IgE level Impact. Second, mice were treated with recombinant IL-4 and their effect on the formation of OVA-specific IgE in serum was observed by increasing the level of exogenous IL-4. Finally, CD40L, TNF-α and IL-13 in peritoneal lymph nodes were detected by semi-quantitative PCR during the formation of IgE in mice immunized with TCS. The trend of gene expression. RESULTS: Anti-IL-4 mAb inhibited TCA-induced OVA-specific IgE formation, but recombinant IL-4 alone did not induce OVA-specific IgE response. High expression peak was observed in the primary and secondary immunization of TCS, and the expression peak of CD40L was similar to that of IL-4, only lasting for a short time. Conclusion: IL-4 is necessary and sufficient for TCS-induced IgE response. CD40L, TNF-α and IL-13 may also be involved in this process, of which CD40L may have the same important role as IL-4.