作者: James Edwards-Smallbone
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摘要: Acanthamoeba castellanii is an amoeboid protozoan which causes opportunistic infections, including granulomatous encephalitis in immune-compromised patients. Haematogenous dissemination follows initial infection and the pathogen exhibits ability to cross blood-brain barrier (BBB). In bloodstream at site of BBB penetration brain microvasculature A. exposed host humoral immunity. Here, we have provided insights into pathogenesis identity amoeba antigens participating immune control. We investigated role circulating immunoglobulin plays preventing BBB, whether trophozoites can alter efficacy response. Furthermore extended previously published data, demonstrating that proteases degrade all antibody classes physiologically-derived antibody. Nonspecific binding polyclonal was also observed, attributed Fc-binding activity by trophozoites. Additionally, examined dynamics under physiological conditions. disruption shown be not directly linked binding, instead it reliant on secreted proteases. This study provides mechanisms evades immunity crosses BBB. This has potential enhance therapeutic strategies aimed restoring essential disease prevention processes. In addition identified a number are targets for system may therefore exploited through vaccination or immunotherapy.