Cryptococcus neoformans is a fungal pathogen that infects the lungs and then often disseminates to the central nervous system, causing meningitis. How Cryptococcus is able to suppress host immunity and escape the antifungal activity of macrophages remains incompletely understood. We reported that the F-box protein Fbp1, a subunit of the SCF(Fbp1) E3 ligase, promotes Cryptococcus virulence by regulating host-Cryptococcus interactions. Our recent studies demonstrated that the fbp1Δ mutant elicited superior protective Th1 host immunity in the lungs and that the enhanced immunogenicity of heat-killed fbp1Δ yeast cells can be harnessed to confer protection against a subsequent infection with the virulent parental strain. We therefore examined the use of heat-killed fbp1Δ cells in several vaccination strategies. Interestingly, the vaccine protection remains effective even in mice depleted of CD4+ T cells. This finding is particularly important in the context of HIV/AIDS-induced immune deficiency. Moreover, we observed that vaccinating mice with heat-killed fbp1Δ induces significant cross-protection against challenge with diverse invasive fungal pathogens, including C. neoformans, C. gattii, and Aspergillus fumigatus, as well as partial protection against Candida albicans Thus, our data suggest that the heat-killed fbp1Δ strain has the potential to be a suitable vaccine candidate against cryptococcosis and other invasive fungal infections in both immunocompetent and immunocompromised populations.IMPORTANCE Invasive fungal infections kill more than 1.5 million people each year, with limited treatment options. There is no vaccine available in clinical use to prevent and control fungal infections. Our recent studies showed that a mutant of the F-box protein Fbp1, a subunit of the SCF(Fbp1) E3 ligase in Cryptococcus neoformans, elicited superior protective Th1 host immunity. Here, we demonstrate that the heat-killed fbp1Δ cells (HK-fbp1) can be harnessed to confer protection against a challenge by the virulent parental strain, even in animals depleted of CD4+ T cells. This finding is particularly important in the context of HIV/AIDS-induced immune deficiency. Moreover, we observed that HK-fbp1 vaccination induces significant cross-protection against challenge with diverse invasive fungal pathogens. Thus, our data suggest that HK-fbp1 has the potential to be a broad-spectrum vaccine candidate against invasive fungal infections in both immunocompetent and immunocompromised populations.

译文

新型隐球菌是一种真菌病原体,会感染肺部,然后经常传播到中枢神经系统,从而引起脑膜炎。隐球菌如何抑制宿主免疫并逃避巨噬细胞的抗真菌活性尚不完全清楚。我们报道了F-box蛋白Fbp1 (SCF(Fbp1) E3连接酶的一个亚基) 通过调节宿主-隐球菌相互作用来促进隐球菌的毒力。我们最近的研究表明,fbp1Δ 突变体在肺部引起了良好的Th1宿主保护性免疫,并且可以利用热杀死的fbp1Δ 酵母细胞增强的免疫原性来保护其免受随后的毒力亲本菌株的感染。因此,我们在几种疫苗接种策略中检查了热杀死的fbp1Δ 细胞的使用。有趣的是,即使在CD4 + T细胞耗尽的小鼠中,疫苗保护仍然有效。在艾滋病毒/艾滋病引起的免疫缺陷的背景下,这一发现尤其重要。此外,我们观察到用热杀死的fbp1Δ 给小鼠接种疫苗会引起对多种侵袭性真菌病原体 (包括新生梭菌,加蒂梭菌和烟曲霉) 的攻击的显着交叉保护,以及对白色念珠菌的部分保护。我们的数据表明,在免疫能力和免疫功能低下的人群中,热灭活的fbp1Δ 菌株有可能成为抗隐球菌病和其他侵袭性真菌感染的合适候选疫苗。侵袭性真菌感染每年杀死超过150万人,治疗选择有限。临床上没有可用的疫苗来预防和控制真菌感染。我们最近的研究表明,新型隐球菌中SCF(Fbp1) E3连接酶的亚基F-box蛋白Fbp1的突变体引起了良好的Th1宿主免疫力。在这里,我们证明了热杀死的fbp1Δ 细胞 (HK-fbp1) 可以被用来保护抵抗强毒力的亲本菌株的挑战,即使在CD4 T细胞耗尽的动物中也是如此。在艾滋病毒/艾滋病引起的免疫缺陷的背景下,这一发现尤其重要。此外,我们观察到HK-fbp1疫苗可诱导针对多种侵袭性真菌病原体的攻击的显着交叉保护。因此,我们的数据表明,在免疫能力和免疫功能低下的人群中,HK-fbp1有可能成为针对侵袭性真菌感染的广谱候选疫苗。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录