Amit Ajay, Dikhit Manas R, Singh Ashish Kumar, Kumar Vikash, Suman Shashi S, Singh Ashu, Kumar Akhilesh, Thakur Ajit Kumar, Das Vidyanand Ravi, Das Pradeep, Bimal Sanjiva
Division of Immunology, Rajendra Memorial Research Institute of Medical Sciences, Patna 800007, India.
Division of Immunology, Rajendra Memorial Research Institute of Medical Sciences, Patna 800007, India; Dept. of Biotechnology, National Institutes of Pharmaceutical Education and Research, Hajipur 844102, India.
Mol Immunol. 2017 Feb;82:104-113. doi: 10.1016/j.molimm.2016.12.022. Epub 2017 Jan 5.
In the present study, the efficacy of Leishmania donovani protein disulfide isomerase (LdPDI) as a DNA vaccine was evaluated in BALB/C mice. Mice immunized with the LdPDI-DNA construct were found to be the most immuno-reactive, as the construct induced higher T-cell proliferation. The increased T-cell proliferation was associated with a substantial rise in Th1 and Th17+ CD4 cell response and triggered a higher proportion of CD8+ T cells for the release of interferon-gamma along with a reduced splenic parasite load on Days20 and 60 post challenge (PC). Furthermore, the vaccine construct triggered increased interferon (IFN)-γ, interleukin(IL)-17A, and IL-22 release accompanied by decreased extracellular signal-regulated kinases (ERK) 1/2 signaling and increased mitogen-activated protein kinase (MAPK) signaling coinciding with an increase in the amount of nitrite and reactive oxygen species (ROS)in vaccinating the splenocyts. We summarize from our data that the PDI-DNA construct of Leishmania donovani has the potential to elicit protective immunity through the pro-inflammatory cytokines of CD8+ and CD4+(Th1 and Th17) following an intervention in the downstream signaling event of ERK1/2 (probably through p38MAPK signaling). Therefore, the study suggests a new control against visceral leishmaniasis in the future.
在本研究中,对杜氏利什曼原虫蛋白二硫键异构酶(LdPDI)作为DNA疫苗在BALB/C小鼠中的疗效进行了评估。发现用LdPDI-DNA构建体免疫的小鼠免疫反应最强,因为该构建体诱导了更高的T细胞增殖。T细胞增殖增加与Th1和Th17 + CD4细胞反应的大幅上升相关,并在攻击后第20天和第60天触发了更高比例的CD8 + T细胞释放干扰素-γ,同时脾脏寄生虫负荷降低。此外,疫苗构建体触发了干扰素(IFN)-γ、白细胞介素(IL)-17A和IL-22释放增加,同时细胞外信号调节激酶(ERK)1/2信号减少,丝裂原活化蛋白激酶(MAPK)信号增加,这与接种脾细胞中亚硝酸盐和活性氧(ROS)量的增加一致。我们从数据中总结出,杜氏利什曼原虫的PDI-DNA构建体有可能在干预ERK1/2的下游信号事件(可能通过p38MAPK信号)后,通过CD8 +和CD4 +(Th1和Th17)的促炎细胞因子引发保护性免疫。因此,该研究为未来内脏利什曼病的防治提出了新方法。