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首页> 外文期刊>Vaccine >The parasite-derived rOv-ASP-1 is an effective antigen-sparing CD4(+) T cell-dependent adjuvant for the trivalent inactivated influenza vaccine, and functions in the absence of MyD88 pathway
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The parasite-derived rOv-ASP-1 is an effective antigen-sparing CD4(+) T cell-dependent adjuvant for the trivalent inactivated influenza vaccine, and functions in the absence of MyD88 pathway

机译：寄生虫衍生的ROV-ASP-1是用于三价灭活流感疫苗的有效抗原 - 抑制CD4（+）T细胞依赖性佐剂，以及在没有MYD88途径的作用

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摘要

Vaccination remains the most cost-effective biomedical approach for controlling influenza disease. In times of pandemics, however, these vaccines cannot be produced in sufficient quantities for worldwide use by the current manufacturing capacities and practices. What is needed is the development of adjuvanted vaccines capable of inducing an adequate or better immune response at a decreased antigen dose. Previously we showed that the protein adjuvant rOv-ASP-1 augments influenza-specific antibody titers and survival after virus challenge in both young adult and old-age mice when administered with the trivalent inactivated influenza vaccine (IIV3). In this study we show that a reduced amount of rOv-ASP-1, with 40-times less IIV3 can also induce protection. Apparently the potency of the rOv-ASP-1 adjuvanted IIV3 vaccine is independent of the IIV3-specific Th1/Th2 associated antibody responses, and independent of the presence of HAI antibodies. However, CD4(+) T helper cells were indispensable for the protection. Further, rOv-ASP-1 with or without IIV3 elicited the increased level of various chemokines, which are known chemoattractant for immune cells, into the muscle 4 h after immunization, and significantly induced the recruitment of monocytes, macrophages and neutrophils into the muscles. The recruited monocytes had higher expression of the activation marker MHCII on their surface as well as CXCR3 and CCR2; receptors for IP-10 and MCP-1, respectively. These results show that the rOvASP-1 adjuvant allows substantial antigen sparing of IIV3 by stimulating at the site of injection the accumulation of chemokines and the recruitment of immune cells that can augment the activation of CDA4(+) T cell immune responses, essential for the production of antibody responses. Protection elicited by the rOvASP-1 adjuvanted IIV3 vaccine also appears to function in the absence of MyD88-signaling. Future studies will attempt to delineate the precise mechanisms by which the rOv-ASP-1 adjuvanted IIV3 vaccine works. (C) 2018 Elsevier Ltd. All rights reserved.
机译：疫苗接种仍然是控制流感疾病最具成本效益的生物医学方法。然而，在流利的时期，这些疫苗不能以足够的数量生产，以便在全球范围内使用目前的制造能力和实践。所需要的是开发辅助疫苗，其能够以降低的抗原剂量诱导足够或更好的免疫应答。此前，我们展示蛋白质佐剂ROV-ASP-1增强了在患有三价灭活流感疫苗（IIV3）的年轻成人和养老鼠中的病毒攻击后病毒攻击后的流感特异性抗体滴度和存活。在这项研究中，我们表明，减少量的Rov-ASP-1，IIV3的40倍也可以诱导保护。显然，ROV-ASP-1佐剂的IIV3疫苗的效力与IIV3特异性TH1 / TH2相关的抗体反应无关，并且与海抗的存在无关。然而，CD4（+）T辅助细胞对于保护是必不可少的。此外，具有或不含IIV3的ROV-ASP-1引发了各种趋化因子的增加的水平，该趋化因子被众所周知的免疫细胞，在免疫后4小时进入肌肉中，并显着诱导单核细胞，巨噬细胞和中性粒细胞募集到肌肉中。募集的单核细胞在它们的表面和CXCR3和CCR2上具有更高的活化标志MHCII表达; IP-10和MCP-1的受体分别。这些结果表明，RoVASP-1佐剂通过在注射率的趋化因子的积累和募集的免疫细胞的募集中促进了可以增加CDA4（+）T细胞免疫反应的募集，允许IIV3的大量抗原诱导。生产抗体反应。由RoVASP-1佐剂的IIV3疫苗引发的保护也似乎在没有MyD88信号传导的情况下起作用。未来的研究将试图描绘ROV-ASP-1佐剂的IIV3疫苗工作的精确机制。 （c）2018年elestvier有限公司保留所有权利。

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