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|Title:||Effects of -arrestin 2 on cytokine production of CD4+ T lymphocytes of mice with allergic asthma|
|Keywords:||Asthma;-arrestin 2;2 adrenergic receptors;CD4+ T lymphocytes;Interleukin-4|
|Abstract:||-arrestin 2 has been shown to participate in the pathogenesis of asthma by inducing Th2 cell migration to the lungs. Whether -arrestin 2 regulates cytokine production of CD4+ T cells is still unknown. The aim of the present study was to investigate the effect of -arrestin 2 on the cytokine production of CD4+ T lymphocytes and the mechanism involved in a mouse model for asthma. After silencing -arrestin 2 expression in CD4+ T lymphocytes from asthmatic mice by RNA interference (RNAi), the interleukin-4 (IL-4) and interferon- (IFN-) levels in CD4+ T lymphocyte culture supernatants with or without terbutaline stimulation were determined. Cell-surface 2 adrenergic receptor (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 -arrestin 2 on both mRNA and protein levels. -arrestin 2 RNAi decreased IL-4 (43.16%) and GATA3 (protein 77.21%, mRNA 62.98%) expression after terbutaline stimulation. Cell-surface 2AR of CD4+ T lymphocytes decreased (15.27%) after terbutaline treatment, but recovered after -arrestin 2 RNAi down-modulation. These findings demonstrate that -arrestin 2 regulates IL-4 production and GATA3 expression of CD4+ T lymphocytes partly through the 2AR signaling pathway in an allergic asthma model.|
|ISSN:||0975-1009 (Online); 0019-5189 (Print)|
|Appears in Collections:||IJEB Vol.49(08) [August 2011]|
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