Stone Brandee L, Brissette Catherine A
Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota , Grand Forks, ND , USA.
Front Immunol. 2017 Jan 19;8:12. doi: 10.3389/fimmu.2017.00012. eCollection 2017.
The emerging pathogen, , is a relapsing fever spirochete vectored by the same species of ticks that carry the causative agents of Lyme disease in the US, Europe, and Asia. Symptoms caused by infection with are similar to a relapsing fever infection. However, has adapted to different vectors and reservoirs, which could result in unique physiology, including immune evasion mechanisms. Lyme utilize a combination of -produced inhibitors and native proteins [i.e., factor H-binding proteins (FHBPs)/complement regulator-acquiring surface proteins, p43, BBK32, BGA66, BGA71, CD59-like protein] to inhibit complement, while some relapsing fever spirochetes use C4b-binding protein and likely -produced inhibitors. To evade the humoral response, utilize antigenic variation of either outer surface proteins (Osps) and the Vmp-like sequences (Vls) system (Lyme borreliae) or variable membrane proteins (Vmps, relapsing fever borreliae). possesses putative FHBPs and antigenic variation of Vmps has been demonstrated. This review summarizes and compares the common mechanisms utilized by Lyme and relapsing fever spirochetes, as well as the current state of understanding immune evasion by .
新出现的病原体——[病原体名称缺失]，是一种复发性发热螺旋体，由在美国、欧洲和亚洲传播莱姆病病原体的同一种蜱作为传播媒介。[病原体名称缺失]感染引起的症状与复发性发热感染相似。然而，[病原体名称缺失]已经适应了不同的传播媒介和宿主，这可能导致其独特的生理特性，包括免疫逃避机制。莱姆螺旋体利用[具体物质名称缺失]产生的抑制剂和天然蛋白质（即因子H结合蛋白（FHBPs）/补体调节因子获取表面蛋白、p43、BBK32、BGA66、BGA71、CD59样蛋白）的组合来抑制补体，而一些复发性发热螺旋体则使用C4b结合蛋白和可能由[具体物质名称缺失]产生的抑制剂。为了逃避体液免疫反应，莱姆螺旋体利用外表面蛋白（Osps）和Vmp样序列（Vls）系统（莱姆疏螺旋体）或可变膜蛋白（Vmps，复发性发热疏螺旋体）的抗原变异。[病原体名称缺失]拥有假定的FHBPs，并且已经证明了Vmps的抗原变异。本综述总结并比较了莱姆螺旋体和复发性发热螺旋体利用的共同机制，以及目前对[病原体名称缺失]免疫逃避的理解现状。
