Reduction of memory Th2 cell pool for the treatment of allergic diseases

哮喘的特征主要由抗原特异性记忆性Th2细胞及其细胞因子IL-4、IL-5和IL-13介导。在这项研究中，我们试图通过DNA微阵列分析和逆转录病毒介导的信号序列陷阱筛选来鉴定记忆性Th2细胞的细胞表面特异性分子。然而，不幸的是，我们不能确定记忆Th2细胞特异性分子在此研究期间。另一方面，我们发现肺中持续的Th2型免疫炎症诱导IL-25的表达和肺动脉重构（PAR）。注射抗IL-25抗体可抑制抗原诱导的PAR。肺特异性IL-25转基因小鼠（CC10 IL-25小鼠）而非CC10 IL-25 NKT ^<-/->小鼠自发地发生PAR。这些结果表明，IL-25在肺中的长期表达通过NKT细胞依赖性机制诱导PAR。

The characteristics of asthma are mainly mediated by antigen-specific memory Th2 cells and their cytokines including IL-4, IL-5, and IL-13. In this study, we tried to identify cell surface molecules specific for memory Th2 cells by using DNA microarray analysis and retrovirus-mediated signal sequence trap screening. However, unfortunately, we could not identify memory Th2 cell-specific molecules within this research period. On the other hand, we found that prolonged Th2-type immune inflammation in the lung induces the expression of IL-25 and pulmonary arterial remodeling (PAR). Injection of anti-IL-25 antibody inhibited antigen-induced PAR. Lung-specificIL-25 transgenic mice (CC10 IL-25 mice) but not CC10 IL-25 NKT^<-/-> mice spontaneouslydeveloped PAR. These results suggest that prolonged expression of IL-25 in the lung induces PARby NKT cell-dependent mechanisms.