Ueno Keigo, Kinjo Yuki, Okubo Yoichiro, Aki Kyoko, Urai Makoto, Kaneko Yukihiro, Shimizu Kiminori, Wang Dan-Ni, Okawara Akiko, Nara Takuya, Ohkouchi Kayo, Mizuguchi Yuki, Kawamoto Susumu, Kamei Katsuhiko, Ohno Hideaki, Niki Yoshihito, Shibuya Kazutoshi, Miyazaki Yoshitsugu
Department of Chemotherapy and Mycoses, National Institute of Infectious Diseases, Tokyo, Japan.
Department of Chemotherapy and Mycoses, National Institute of Infectious Diseases, Tokyo, Japan
Infect Immun. 2015 Apr;83(4):1577-86. doi: 10.1128/IAI.02827-14. Epub 2015 Feb 2.
Cryptococcosis due to a highly virulent fungus, Cryptococcus gattii, emerged as an infectious disease on Vancouver Island in Canada and surrounding areas in 1999, causing deaths among immunocompetent individuals. Previous studies indicated that C. gattii strain R265 isolated from the Canadian outbreak had immune avoidance or immune suppression capabilities. However, protective immunity against C. gattii has not been identified. In this study, we used a gain-of-function approach to investigate the protective immunity against C. gattii infection using a dendritic cell (DC)-based vaccine. Bone marrow-derived dendritic cells (BMDCs) efficiently engulfed acapsular C. gattii (Δcap60 strain), which resulted in their expression of costimulatory molecules and inflammatory cytokines. This was not observed for BMDCs that were cultured with encapsulated strains. When Δcap60 strain-pulsed BMDCs were transferred to mice prior to intratracheal R265 infection, significant amelioration of pathology, fungal burden, and the survival rate resulted compared with those in controls. Multinucleated giant cells (MGCs) that engulfed fungal cells were significantly increased in the lungs of immunized mice. Interleukin 17A (IL-17A)-, gamma interferon (IFN-γ)-, and tumor necrosis factor alpha (TNF-α)-producing lymphocytes were significantly increased in the spleens and lungs of immunized mice. The protective effect of this DC vaccine was significantly reduced in IFN-γ knockout mice. These results demonstrated that an increase in cytokine-producing lymphocytes and the development of MGCs that engulfed fungal cells were associated with the protection against pulmonary infection with highly virulent C. gattii and suggested that IFN-γ may have been an important mediator for this vaccine-induced protection.
由高毒力真菌加氏隐球菌引起的隐球菌病于1999年在加拿大温哥华岛及周边地区作为一种传染病出现,导致免疫功能正常的个体死亡。先前的研究表明,从加拿大疫情中分离出的加氏隐球菌R265菌株具有免疫逃避或免疫抑制能力。然而,尚未确定针对加氏隐球菌的保护性免疫。在本研究中,我们采用功能获得方法,使用基于树突状细胞(DC)的疫苗来研究针对加氏隐球菌感染的保护性免疫。骨髓来源的树突状细胞(BMDC)有效地吞噬了无荚膜加氏隐球菌(Δcap60菌株),这导致它们表达共刺激分子和炎性细胞因子。用有荚膜菌株培养的BMDC则未观察到这种情况。当在气管内接种R265之前将经Δcap60菌株脉冲处理的BMDC转移到小鼠体内时,与对照组相比,病理、真菌负荷和存活率均有显著改善。免疫小鼠肺部吞噬真菌细胞的多核巨细胞(MGC)显著增加。免疫小鼠的脾脏和肺部中产生白细胞介素17A(IL-17A)、γ干扰素(IFN-γ)和肿瘤坏死因子α(TNF-α)的淋巴细胞显著增加。在IFN-γ基因敲除小鼠中,这种DC疫苗的保护作用显著降低。这些结果表明,产生细胞因子的淋巴细胞增加以及吞噬真菌细胞的MGC的发育与针对高毒力加氏隐球菌肺部感染的保护作用相关,并表明IFN-γ可能是这种疫苗诱导的保护作用的重要介质。