Abstract
Our previous study demonstrated that splenic NK cell activities were significantly higher in the EA-treated rats than in the non-acupunctured rats, and that lesion of the lateral hypothalamic area (LHA) abolished the effects of EA on NK cell activity. We also examined EA-induced alterations of gene expression in splenic NK cells using microarray technique and real time RT-PCR. Our data shows that EA treatment increased CD94, PTK and VCAM-1 expressions while decreased PTP and SHP-1. In additional sets of experiments, we showed that successive EA treatment reduces IgE production in BALB/c mice immunized with 2,4-dinitrophenylated keyhole limpet protein (DNP-KLH) by suppression of the Th2 cell lineage development. Furthermore, pretreatment of phentolamine (α-adrenergic receptor antagonist) or Y-25130 (5-HT3 receptor antagonist), but not naloxone (general opioid receptor antagonist), completely blocks the EA-induced suppression of antigen-specific and total IgE levels in serum, and IL-4 production in anti-CD3 mAb-activated splenocytes in DNP-KLH immunized mice. Therefore, it is suggested that EA modulate NK cell activities and Th1/Th2 cell responses through the neural-immune interaction.This work was supported by the SRC program of KOSEF (R11-2005-014), Republic of Korea. [J Physiol Sci. 2008;58 Suppl:S8]
