炎症体
吡喃结构域
神经退行性变
小胶质细胞
先天免疫系统
细胞生物学
生物
神经科学
神经炎症
免疫系统
疾病
医学
炎症
免疫学
病理
作者
Michael T. Heneka,Róisín M. McManus,Eicke Latz
标识
DOI:10.1038/s41583-018-0055-7
摘要
The mammalian CNS is an intricate and fragile structure, which on one hand is open to change in order to store information, but on the other hand is vulnerable to damage from injury, pathogen invasion or neurodegeneration. During senescence and neurodegeneration, activation of the innate immune system can occur. Inflammasomes are signalling complexes that regulate cells of the immune system, which in the brain mainly includes microglial cells. In microglia, the NLRP3 (NOD-, LRR- and pyrin domain-containing 3) inflammasome becomes activated when these cells sense proteins such as misfolded or aggregated amyloid-β, α-synuclein and prion protein or superoxide dismutase, ATP and members of the complement pathway. Several other inflammasomes have been described in microglia and the other cells of the brain, including astrocytes and neurons, where their activation and subsequent caspase 1 cleavage contribute to disease development and progression.
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