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Mechanisms of immune evasion in fungal pathogens

机译:真菌病原体免疫逃逸的机制

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摘要

The incidence of life-threatening fungal infections has continued to increase in recent years, predominantly in patients debilitated by iatrogenic interventions or immunological dysfunctions. While the picture of the immunology of fungal infections grows increasingly complex, it is clear that the phagocyte-pathogen interaction is a critical determinant of establishing an infection. About 10 years ago, genome-scale approaches began to elucidate the intricate and extensive fungal response to phagocytosis and in the last few years it has become clear that some of this response actively modulates immune cell function. Fungal pathogens avoid detection by masking pathogen-associated molecular patterns, such as cell wall carbohydrates, and by downregulating the complement cascade. Once detected, various species interfere with phagocytosis and intracellular trafficking, and can repress production of antimicrobials like nitric oxide (NO). For the most part, the molecular mechanisms behind these behaviors are not yet known. This review discusses recent discoveries and insights into how fungi manipulate the host-pathogen interaction.
机译:近年来,威胁生命的真菌感染的发生率持续增加,主要发生在医源性干预或免疫功能障碍使患者虚弱的患者中。尽管真菌感染的免疫学图片变得越来越复杂,但很明显吞噬细胞与病原体的相互作用是建立感染的关键因素。大约10年前,基因组规模的方法开始阐明对吞噬作用的复杂而广泛的真菌反应,并且在最近几年中,已经清楚地表明某些这种反应可以主动调节免疫细胞的功能。真菌病原体通过掩盖病原体相关的分子模式(例如细胞壁碳水化合物)以及下调补体级联反应来避免检测。一旦被检测到,各种物种就会干扰吞噬作用和细胞内运输,并会抑制一氧化氮(NO)等抗菌药物的产生。在大多数情况下,这些行为背后的分子机制尚不清楚。这篇评论讨论了最近的发现和对真菌如何操纵宿主-病原体相互作用的见解。

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