Roles of Th9 cells in the development of allergic glanulomatous angitis and asthma

最近的研究表明，肺部持续的th2型免疫炎症可诱导肺动脉重塑。然而，促进th2型炎症的IL-25在肺动脉重塑发展中的作用尚不清楚。在这项研究中，我们评估了IL-25在肺动脉重塑发展中的作用。反复吸入OVA致敏小鼠肺动脉壁增厚及肺组织IL-25和RELMa mRNA的表达。注射中和性抗il -25抗体可抑制ova诱导的肺动脉壁增厚及肺组织中RELMa的表达。CC10 IL-25小鼠而非CC10 IL-25 NKT-/-小鼠在6月龄时自发出现肺动脉壁增厚和肺部RELMa表达。这些结果表明，延长IL-25在肺中的表达通过依赖NKT细胞的机制诱导肺动脉壁增厚。

Recent studies have shown that prplonged Th2-type immune inflammation in the lung induces pulmonary arterial remodeling. However, roles of IL-25, which promotes Th2-type inflammation, in the development of pulmonary arterial remodeling remain unknown. In this study, we evaluated the role of IL-25 in the development of pulmonary arterial remodeling. Repeated OVA inhalation induced pulmonary arterial wall thickening and the expression of IL-25 and RELMa mRNA in the lung in OVA-sensitized mice. Injection of neutralizing anti-IL-25 antibody inhibited OVA-induced pulmonary arterial wall thickening and RELMa expression in the lung. CC10 IL-25 mice but not CC10 IL-25 NKT-/- mice spontaneously developed pulmonary arterial wall thickening and RELMa expression in the lung at 6 months of age. These results shows that prolonged expression of IL-25 in the lung induces pulmonary arterial wall thickening by NKT cell-dependent mechanisms.