期刊
NATURE IMMUNOLOGY
卷 9, 期 8, 页码 857-865出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1636
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- NIAID NIH HHS [R01 AI065483, AI065483] Funding Source: Medline
- NIA NIH HHS [R01 AG020255, R01 AG020255-06A1, AG20255] Funding Source: Medline
- NIGMS NIH HHS [GM54060, R37 GM054060, R01 GM054060] Funding Source: Medline
The fibrillar peptide amyloid-beta (A beta) has a chief function in the pathogenesis of Alzheimer's disease. Interleukin 1 beta (IL-1 beta) is a key cytokine in the inflammatory response to A beta. Insoluble materials such as crystals activate the inflammasome formed by the cytoplasmic receptor NALP3, which results in the release of IL-1 beta. Here we identify the NALP3 inflammasome as a sensor of A beta in a process involving the phagocytosis of A beta and subsequent lysosomal damage and release of cathepsin B. Furthermore, the IL-1 beta pathway was essential for the microglial synthesis of proinflammatory and neurotoxic factors, and the inflammasome, caspase-1 and IL-1 beta were critical for the recruitment of microglia to exogenous A beta in the brain. Our findings suggest that activation of the NALP3 inflammasome is important for inflammation and tissue damage in Alzheimer's disease.
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