PDF(Pubmed)
Abstract：
Leishmania donovani surface glycoprotein 63 (GP63) is a major virulence factor involved in parasite escape and immune evasion. In this study, we generated virus-like particles (VLPs) expressing L. donovani GP63 using the baculovirus expression system. Mice were intramuscularly immunized with GP63-VLPs and challenged with L. donovani promastigotes. GP63-VLP immunization elicited higher levels of L. donovani antigen-specific serum antibodies and enhanced splenic B cell, germinal center B cell, CD4+, and CD8+ T cell responses compared to unimmunized controls. GP63-VLPs inhibited the influx of pro-inflammatory cytokines IFN-γ and IL-6 in the livers, as well as thwarting the development of splenomegaly in immunized mice. Upon L. donovani challenge infection, a drastic reduction in splenic parasite burden was observed in VLP-immunized mice. These results indicate that GP63-VLPs immunization conferred protection against L. donovani challenge infection by inducing humoral and cellular immunity in mice.
摘要：
杜氏利什曼原虫表面糖蛋白63（GP63）是参与寄生虫逃逸和免疫逃避的主要毒力因子。在这项研究中,我们使用杆状病毒表达系统产生了表达多氏乳杆菌GP63的病毒样颗粒（VLP）。用GP63-VLP对小鼠进行肌内免疫,并用多诺瓦尼乳杆菌原刺激。GP63-VLP免疫引起更高水平的多尼氏乳杆菌抗原特异性血清抗体和增强的脾B细胞,生发中心B细胞，CD4+,和与未免疫对照相比的CD8+T细胞应答。GP63-VLP抑制肝脏中促炎细胞因子IFN-γ和IL-6的流入,以及阻止免疫小鼠脾肿大的发展。在多诺瓦尼乳杆菌攻击感染后，在VLP免疫小鼠中观察到脾寄生虫负荷的急剧减少.这些结果表明,GP63-VLP免疫通过在小鼠中诱导体液和细胞免疫而赋予针对多氏乳杆菌攻击感染的保护。
