QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Front Immunol. 2018 Dec 14;9:2926. doi: 10.3389/fimmu.2018.02926. eCollection 2018.
spp., the causative agent of malaria, caused 212 million infections in 2016 with 445,000 deaths, mostly in children. Adults acquire enough immunity to prevent clinical symptoms but never develop sterile immunity. The only vaccine for malaria, RTS,S, shows promising protection of a limited duration against clinical malaria in infants but no significant protection against severe disease. There is now abundant evidence that T cell functions are inhibited during malaria, which may explain why vaccine are not efficacious. Studies have now clearly shown that T cell immunity against malaria is subdued by multiple the immune regulatory receptors, in particular, by programmed cell-death-1 (PD-1). Given there is an urgent need for an efficacious malarial treatment, compounded with growing drug resistance, a better understanding of malarial immunity is essential. This review will examine molecular signals that affect T cell-mediated immunity against malaria.
疟原虫 spp. 是疟疾的病原体,2016 年导致了 2.12 亿例感染和 44.5 万人死亡,其中大多数是儿童。成年人获得了足够的免疫力来预防临床症状,但从未产生无菌免疫力。唯一的疟疾疫苗 RTS,S 在预防婴儿临床疟疾方面显示出有希望的有限保护作用,但对严重疾病没有显著保护作用。现在有大量证据表明,疟疾期间 T 细胞功能受到抑制,这可能解释了为什么疫苗无效。研究现在已经清楚地表明,T 细胞对疟疾的免疫受到多种免疫调节受体的抑制,特别是程序性细胞死亡-1(PD-1)。鉴于急需有效的疟疾治疗方法,再加上耐药性不断增加,因此更好地了解疟疾免疫至关重要。这篇综述将探讨影响 T 细胞介导的抗疟疾免疫的分子信号。