Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 10 3 2011 09 15 171 182 EN Yi Liu Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China Gu-yi Wang Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China Shao-kun Liu Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China Mu-yi Yang Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China Li-bing Ma Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China Keng Li Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China Su-bo Gong Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China Li Zhang Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China Ping Chen Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China Xu-dong Xiang Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China 2015 10 01 Allergic asthma is a complex and chronic inflammatory airway disease. Interleukin-17 is a pro-inflammatory cytokine which plays critical role in the pathogenesis of allergic asthma. It has been reported that β-arrestin2 regulated the development of allergic asthma at a proximal step in the inflammatory cascade. In this study, the influence of β-arrestin2 on Interleukin-17 production and expression of CD4+  T lymphocytes in a murine asthma model was investigated. Splenic CD4+   T lymphocytes from  wild-type mice and those  from  a murine asthma model were purified. CD4+  T lymphocytes from a murine asthma model were transfected with  siRNAs  targeting the  β-arrestin2  or  were pretreated  with  the  ERK1/2  inhibitor,PD98059.  After  stimulation,  the   protein   expression  of   β-arrestin2、phosphorylated- ERK1/2 and IL-17 were detection by Western blot; the mRNA expression of IL-17 were detected by real-time PCR; the accumulation of IL-17 in supernatants  were detected by ELISA. We found that β-arrestin2、phosphorylated-ERK1/2 and IL-17 expression in CD4+  T lymphocytes from a murine asthma model was increased compared with those from wild- type mice(p<0.01). Treatment of CD4+  T lymphocytes with siRNAs targeting the β-arrestin2 down-regulated phosphorylated-  ERK  1/2  and  IL-17 expression  (p <  0.01). PD98059 decreased IL-17 production  and expression in CD4+   T lymphocytes in a murine asthma model (p < 0.05). We conclude that β-arrestin2 stimulated IL-17 production  and expression of CD4+   T lymphocytes in a murine  asthma  model. The  effect  was partly mediated  by ERK  1/2 activation. Targeting β-arrestin2 biological activity could be a valid therapeutic approach for the treatment of allergic asthma. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/308 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/308/308