Hayashi T, Maeda K, Hasegawa K, Nakai S, Hamachi T, Iwata H
Laboratories of Veterinary Pathology, Faculty of Agriculture, Yamaguchi University, Japan.
Int J Exp Pathol. 2002 Apr;83(2):81-6. doi: 10.1046/j.1365-2613.2002.00218.x.
Asthma might be caused by a helper T(Th)2 immune response. We hypothesized that the systemic administration of the Th1 cytokines may reduce the Th2 type late asthmatic response (LAR). We examined the effect of the intraperitoneal injection of interferon(IFN)-gamma-expressing plasmid, a Th1 cytokine, or interleukin(IL)-4-expressing plasmid, a Th2 cytokine, at the time of sensitization on a mouse model of asthma induced by ovalbumin in BALB/c mice. We demonstrated that the IFN-gamma-expressing plasmid reduced the LAR, whereas the IL-4-expressing plasmid enhanced the LAR as compared with the saline or plasmid-only treated group. The present study suggests that the systemic administration of IFN-gamma-expressing plasmid may have a modulating ability of Th1/Th2 balance to down-regulate Th2 response by a mutual inhibitory mechanism between Th1 and Th2 cells, leading to the reduction of the LAR.
哮喘可能由辅助性T(Th)2免疫反应引起。我们推测,全身给予Th1细胞因子可能会减轻Th2型迟发性哮喘反应(LAR)。我们研究了在致敏时腹腔注射表达Th1细胞因子γ干扰素(IFN)的质粒或表达Th2细胞因子白细胞介素(IL)-4的质粒对卵清蛋白诱导的BALB/c小鼠哮喘模型的影响。我们发现,与生理盐水或仅注射质粒的处理组相比,表达IFN-γ的质粒减轻了LAR,而表达IL-4的质粒增强了LAR。本研究表明,全身给予表达IFN-γ的质粒可能具有调节Th1/Th2平衡的能力,通过Th1和Th2细胞之间的相互抑制机制下调Th2反应,从而减轻LAR。