Probst Peter, Grigg John B, Wang Myra, Muñoz Ernesto, Loo Yueh-Ming, Ireton Renee C, Gale Michael, Iadonato Shawn P, Bedard Kristin M
Kineta, Inc., 219 Terry Ave. N., Seattle, WA 98109, USA.
Department of Immunology, University of Washington, Seattle, WA 98195, USA; Center for Innate Immunity and Immune Disease, University of Washington, Seattle, WA 98195, USA.
Vaccine. 2017 Apr 4;35(15):1964-1971. doi: 10.1016/j.vaccine.2017.01.053. Epub 2017 Mar 6.
Vaccine adjuvants are essential to drive a protective immune response in cases where vaccine antigens are weakly immunogenic, where vaccine antigen is limited, or where an increase in potency is needed for a specific population, such as the elderly. To discover novel vaccine adjuvants, we used a high-throughput screen (HTS) designed to identify small-molecule agonists of the RIG-I-like receptor (RLR) pathway leading to interferon regulatory factor 3 (IRF3) activation. RLRs are a group of cytosolic pattern-recognition receptors that are essential for the recognition of viral nucleic acids during infection. Upon binding of viral nucleic acid ligands, the RLRs become activated and signal to transcription factors, including IRF3, to initiate an innate immune transcriptional program to control virus infection. Among our HTS hits were a series of benzothiazole compounds from which we designed the lead analog, KIN1148. KIN1148 induced dose-dependent IRF3 nuclear translocation and specific activation of IRF3-responsive promoters. Prime-boost immunization of mice with a suboptimal dose of a monovalent pandemic influenza split virus H1N1 A/California/07/2009 vaccine plus KIN1148 protected against a lethal challenge with mouse-adapted influenza virus (A/California/04/2009) and induced an influenza virus-specific IL-10 and Th2 response by T cells derived from lung and lung-draining lymph nodes. Prime-boost immunization with vaccine plus KIN1148, but not prime immunization alone, induced antibodies capable of inhibiting influenza virus hemagglutinin and neutralizing viral infectivity. Nevertheless, a single immunization with vaccine plus KIN1148 provided increased protection over vaccine alone and reduced viral load in the lungs after challenge. These findings suggest that protection was at least partially mediated by a cellular immune component and that the induction of Th2 and immunoregulatory cytokines by a KIN1148-adjuvanted vaccine may be particularly beneficial for ameliorating the immunopathogenesis that is associated with influenza viruses.
疫苗佐剂对于在疫苗抗原免疫原性较弱、疫苗抗原有限或特定人群(如老年人)需要提高效力的情况下引发保护性免疫反应至关重要。为了发现新型疫苗佐剂,我们使用了一种高通量筛选(HTS)方法,旨在识别导致干扰素调节因子3(IRF3)激活的视黄酸诱导基因I样受体(RLR)途径的小分子激动剂。RLR是一组胞质模式识别受体,在感染期间识别病毒核酸至关重要。在与病毒核酸配体结合后,RLR被激活并向包括IRF3在内的转录因子发出信号,启动先天免疫转录程序以控制病毒感染。在我们的高通量筛选命中物中,有一系列苯并噻唑化合物,我们从中设计了先导类似物KIN1148。KIN1148诱导剂量依赖性的IRF3核转位和IRF3反应性启动子的特异性激活。用次优剂量的单价大流行性流感裂解病毒H1N1 A/California/07/2009疫苗加KIN1148对小鼠进行初免-加强免疫,可保护小鼠免受适应小鼠的流感病毒(A/California/04/2009)的致死性攻击,并诱导来自肺和引流肺淋巴结的T细胞产生流感病毒特异性IL-10和Th2反应。用疫苗加KIN1148进行初免-加强免疫,但单独初免则不能,可诱导能够抑制流感病毒血凝素并中和病毒感染性的抗体。然而,用疫苗加KIN1148进行单次免疫比单独使用疫苗提供了更高的保护,并在攻击后降低了肺中的病毒载量。这些发现表明,保护至少部分是由细胞免疫成分介导的,并且KIN1148佐剂疫苗诱导的Th2和免疫调节细胞因子可能对改善与流感病毒相关的免疫发病机制特别有益。