Effects of β-arrestin 2 on cytokine production of CD4

β-arrestin 2 has been shown to participate in the pathogenesis of asthma by inducing Th2 cell migration to the lungs. Whether β-arrestin 2 regulates cytokine production of CD4 T cells is still unknown. The aim of the present study was to investigate the effect of β-arrestin 2 on the cytokine production of CD4 T lymphocytes and the mechanism involved in a mouse model for asthma. After silencing β-arrestin 2 expression in CD4 T lymphocytes from asthmatic mice by RNA interference (RNAi), the interleukin-4 (IL-4) and interferon-γ (IFN-γ) levels in CD4 T lymphocyte culture supernatants with or without terbutaline stimulation were determined. Cell-surface β2 adrenergic receptor (β2AR) as well as GATA3 expression of CD4 T lymphocytes were also measured. CD4 T lymphocytes of mice with allergic asthma expressed higher levels of β-arrestin 2 on both mRNA and protein levels. β-arrestin 2 RNAi decreased IL-4 (43.16%) and GATA3 (protein 77.21%, mRNA 62.98%) expression after terbutaline stimulation. Cell-surface β2AR of CD4 T lymphocytes decreased (15.27%) after terbutaline treatment, but recovered after β-arrestin 2 RNAi down-modulation. These findings demonstrate that β-arrestin 2 regulates IL-4 production and GATA3 expression of CD4 T lymphocytes partly through the β2AR signaling pathway in an allergic asthma model.