β-arrestin2 Stimulates Interleukin-17 Production and Expression of CD4+ T Lymphocytes in a Murine Asthma Model

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 -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 -βarrestin2 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 byelisa.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 wildtype 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