临床上发现肺炎支原体感染的患儿常常表现为咳喘，并且常继发过敏性疾病。我们的一项前期研究表明肺炎支原体感染的患儿血清中IgE水平显著升高，且Th1/Th2类细胞因子发生失衡。已有研究表明Jak/STAT信号通路调控Th细胞的分化。由此我们推断肺炎支原体感染后是通过Jak/STAT信号通路来调节Th0细胞的分化，并最导致Th1/Th2类细胞因子的失衡，引起哮喘等过敏性疾病。因此，本课题拟通过建立肺炎支原体感染的小鼠模型及将肺炎支原体与Naïve T细胞进行共培养，检测信号通路中关键分子以及细胞因子水平的变化来验证上述想法。此外，本课题还拟通过分离肺炎支原体不同的菌体成分与Naïve T细胞进行共培养以明确引起Th细胞分化的有效病原成分。本课题有望为肺炎支原体引起哮喘的发病提供卫生学证据，为疫苗的研制提供靶点。

In clinical practice, we found that children with mycoplasma pneumoniae infection are often characterized by cough and inspiratory wheeze, and often develop secondary allergic disease. Our previous study showed that when children with mycoplasma pneumoniae infection there are significant increasement in serum IgE levels, and there are Th1/Th2 cytokines imbalances. We want to know the exact signal pathway to work. The existing studies have shown that Jak/STAT signaling pathways regulate the differentiation of Th cells. Hence we infer that mycoplasma pneumoniae infection is through the Jak/STAT signaling pathway to regulate Th0 cell differentiation, and ultimately causes the imbalance of Th1/Th2 cytokines, then induces allergic disease such as asthma. Therefore, this study plans to establish mycoplasma pneumoniae infection model in mice and to use the mycoplasma pneumoniae to co-culture with Naive T cells, then to test key molecules in the signal pathways and cytokine levels to verify the above idea. In addition, this study plans to separate different ingredients of mycoplasma pneumoniae to co-culture with Naive T cells in order to make clear the specific composition which to influence Th cell differentiation. This study is expected to provide hygiene evidence for the hypothesis that mycoplasma pneumoniae can cause asthma and to provide targets for vaccines.