Effects of <img src='/image/spc_char/beta.gif' border=0>-arrestin 2 on cytokine production of CD4+ T lymphocytes of mice with allergic asthma

Abstract

<img src='/image/spc_char/beta.gif' border=0>-arrestin 2 has been shown to participate in the pathogenesis of asthma by inducing Th2 cell migration to the lungs. Whether <img src='/image/spc_char/beta.gif' border=0>-arrestin 2 regulates cytokine production of CD4+ T cells is still unknown. The aim of the present study was to investigate the effect of <img src='/image/spc_char/beta.gif' border=0>-arrestin 2 on the cytokine production of CD4+ T lymphocytes and the mechanism involved in a mouse model for asthma. After silencing <img src='/image/spc_char/beta.gif' border=0>-arrestin 2 expression in CD4+ T lymphocytes from asthmatic mice by RNA interference (RNAi), the interleukin-4 (IL-4) and interferon-<img src='/image/spc_char/gamma2.gif' border=0> (IFN-<img src='/image/spc_char/gamma2.gif' border=0>) levels in CD4+ T lymphocyte culture supernatants with or without terbutaline stimulation were determined. Cell-surface <img src='/image/spc_char/beta.gif' border=0>2 adrenergic receptor (<img src='/image/spc_char/beta.gif' border=0>2AR) as well as GATA3 expression of CD4+ T lymphocytes were also measured. CD4+ T lymphocytes of mice with allergic asthma expressed higher levels of <img src='/image/spc_char/beta.gif' border=0>-arrestin 2 on both mRNA and protein levels. <img src='/image/spc_char/beta.gif' border=0>-arrestin 2 RNAi decreased IL-4 (43.16%) and GATA3 (protein 77.21%, mRNA 62.98%) expression after terbutaline stimulation. Cell-surface <img src='/image/spc_char/beta.gif' border=0>2AR of CD4+ T lymphocytes decreased (15.27%) after terbutaline treatment, but recovered after <img src='/image/spc_char/beta.gif' border=0>-arrestin 2 RNAi down-modulation. These findings demonstrate that <img src='/image/spc_char/beta.gif' border=0>-arrestin 2 regulates IL-4 production and GATA3 expression of CD4+ T lymphocytes partly through the <img src='/image/spc_char/beta.gif' border=0>2AR signaling pathway in an allergic asthma model.