Department of Microbiology and Immunology, School of Medicine, Pusan National University, yangsan 626-770, Korea.
BMB Rep. 2012 Feb;45(2):79-84. doi: 10.5483/BMBRep.2012.45.2.79.
In asthma, T helper 2 (T(H)2)-type cytokines such as interleukin (IL)-4, IL-5, and IL-13 are produced by activated CD4(+) T cells. Dendritic cells played an important role in determining the fate of naive T cells into either T(H)1 or T(H)2 cells. We determined whether RG-II regulates the T(H)1/T(H)2 immune response by using an ovalbumin-induced murine model of asthma. RG-II reduced IL-4 production but increased interferon- gamma production, and inhibited GATA-3 gene expression. RG-II also inhibited asthmatic reactions including an increase in the number of eosinophils in bronchoalveolar lavage fluid, an increase in inflammatory cell infiltration in lung tissues, airway luminal narrowing, and airway hyperresponsiveness. This study provides evidence that RG-II plays a critical role in ameliorating the pathogenic process of asthmatic inflammation in mice. These findings provide new insights into the immunotherapeutic role of RG-II in terms of its effects in a murine model of asthma.
在哮喘中,辅助性 T 细胞 2(T(H)2)-型细胞因子,如白细胞介素(IL)-4、IL-5 和 IL-13,由激活的 CD4(+) T 细胞产生。树突状细胞在决定初始 T 细胞向 T(H)1 或 T(H)2 细胞分化的命运方面发挥着重要作用。我们通过卵清蛋白诱导的哮喘小鼠模型来确定 RG-II 是否通过调节 T(H)1/T(H)2 免疫反应来发挥作用。RG-II 减少了白细胞介素-4 的产生,但增加了干扰素-γ的产生,并抑制了 GATA-3 基因的表达。RG-II 还抑制了哮喘反应,包括支气管肺泡灌洗液中嗜酸性粒细胞数量的增加、肺组织中炎症细胞浸润的增加、气道腔狭窄和气道高反应性。这项研究提供了证据,表明 RG-II 在改善哮喘小鼠炎症发病机制中起着关键作用。这些发现为 RG-II 在哮喘小鼠模型中的免疫治疗作用提供了新的见解。