Crosstalk Between Autophagy and Hypoxia-Inducible Factor-1α in Antifungal Immunity.
Crosstalk Between Autophagy and Hypoxia-Inducible Factor-1α in Antifungal Immunity.
复制标题
抗真菌免疫中自噬与缺氧诱导因子-1 α的相互作用
作者：
Quäschling T;Friedrich D;Deepe GS Jr;Rupp J
现代医学受到几种潜在的严重真菌病原体的挑战，如烟曲霉、白色念珠菌或荚膜组织胞浆菌。虽然不是所有的真菌病原体都进化为主要病原体，但机会性病原体仍然可以在免疫功能低下的患者中引起致命的感染。在感染这些真菌后，先天免疫细胞的摄取和清除是宿主免疫应答的重要部分。天然免疫细胞利用两种不同的自噬途径，经典途径和非经典途径，也称为微管相关蛋白1A/1B-轻链3（LC 3）-相关途径（microtubule-associated protein 1A/1B-light chain 3，LC 3-associated pathway，LC 3），从细胞内环境中清除真菌病原体。自噬相关的宿主免疫应答的结果取决于病原体和细胞类型。因此，了解自噬的潜在分子机制对于开发和改进抗真菌疗法至关重要。其中一个分子机制是转录因子缺氧诱导因子1α（HIF-1α）与自噬免疫反应的相互作用。在这篇综述中，我们将集中在自噬和HIF-1α对真菌感染结果的作用的全面概述。
Modern medicine is challenged by several potentially severe fungal pathogens such as Aspergillus fumigatus, Candida albicans, or Histoplasma capsulatum. Though not all fungal pathogens have evolved as primary pathogens, opportunistic pathogens can still cause fatal infections in immuno-compromised patients. After infection with these fungi, the ingestion and clearance by innate immune cells is an important part of the host immune response. Innate immune cells utilize two different autophagic pathways, the canonical pathway and the non-canonical pathway, also called microtubule-associated protein 1A/1B-light chain 3 (LC3) -associated pathway (LAP), to clear fungal pathogens from the intracellular environment. The outcome of autophagy-related host immune responses depends on the pathogen and cell type. Therefore, the understanding of underlying molecular mechanisms of autophagy is crucial for the development and improvement of antifungal therapies. One of those molecular mechanisms is the interaction of the transcription-factor hypoxia-inducible factor 1α (HIF-1α) with the autophagic immune response. During this review, we will focus on a comprehensive overview of the role of autophagy and HIF-1α on the outcome of fungal infections.
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选择性自噬：异种。
影响因子：
4.8
作者：
Bauckman, Kyle A.;Owusu-Boaitey, Nana;Mysorekar, Indira U.
通讯作者：
Mysorekar, Indira U.
影响因子：
6.7
作者：
Brothers KM;Gratacap RL;Barker SE;Newman ZR;Norum A;Wheeler RT
通讯作者：
Wheeler RT
影响因子：
4
作者：
Zhang X;Mardinoglu A;Joosten LAB;Kuivenhoven JA;Li Y;Netea MG;Groen AK
通讯作者：
Groen AK
影响因子：
20.1
作者：
Jung, F;Palmer, LA;Johns, RA
通讯作者：
Johns, RA
影响因子：
5.5
作者：
Itakura, Asako;McCarty, Owen J. T.
通讯作者：
McCarty, Owen J. T.