Inflammasomes in neuroinflammatory and neurodegenerative diseases.,EMBO Molecular Medicine

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Inflammasomes in neuroinflammatory and neurodegenerative diseases.
EMBO Molecular Medicine ( IF 9.0 ) Pub Date : 2019-06-01 , DOI: 10.15252/emmm.201810248
Sofie Voet _{1,

2} , Sahana Srinivasan _{1,

2} , Mohamed Lamkanfi _{3,

4} , Geert van Loo _{2,

5}

Affiliation

Neuroinflammation and neurodegeneration often result from the aberrant deposition of aggregated host proteins, including amyloid-β, α-synuclein, and prions, that can activate inflammasomes. Inflammasomes function as intracellular sensors of both microbial pathogens and foreign as well as host-derived danger signals. Upon activation, they induce an innate immune response by secreting the inflammatory cytokines interleukin (IL)-1β and IL-18, and additionally by inducing pyroptosis, a lytic cell death mode that releases additional inflammatory mediators. Microglia are the prominent innate immune cells in the brain for inflammasome activation. However, additional CNS-resident cell types including astrocytes and neurons, as well as infiltrating myeloid cells from the periphery, express and activate inflammasomes. In this review, we will discuss current understanding of the role of inflammasomes in common degenerative diseases of the brain and highlight inflammasome-targeted strategies that may potentially treat these diseases.

中文翻译：

神经炎性和神经退行性疾病中的炎症小体。

神经炎症和神经变性通常是由聚集的宿主蛋白异常沉积引起的，包括淀粉样蛋白-β，α-突触核蛋白和病毒，它们可以激活炎症小体。炎性小体充当微生物病原体和外来的以及宿主衍生的危险信号的细胞内传感器。激活后，它们通过分泌炎性细胞因子白介素（IL）-1β和IL-18诱导先天免疫反应，此外还诱导细胞凋亡，这是一种释放额外炎症介质的裂解细胞死亡模式。小胶质细胞是大脑中炎性体激活的主要先天免疫细胞。但是，包括星形胶质细胞和神经元在内的其他中枢神经系统驻留细胞类型，以及从周围细胞浸润的髓样细胞，都可以表达并激活炎症小体。在这篇评论中，

更新日期：2019-11-06

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