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Comment
. 2008 Aug;9(8):831-3.
doi: 10.1038/ni0808-831.

NLRs and the dangers of pollution and aging

Stephen B Willingham, Jenny P-Y Ting
Comment

NLRs and the dangers of pollution and aging

Stephen B Willingham et al. Nat Immunol. 2008 Aug.

Abstract

Inflammatory interleukin 1β production after silica and alum crystal or β-amyloid uptake occurs via a process involving lysosomal destabilization and release of cathepsin B that activates the NALP3 inflammasome.

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Figures

Figure 1
Figure 1. Lysosomal permeabilization activates the NLRP3 inflammasome
Phagocytosis of silica crystals, aluminum salts, or β–amyloid fibrils results in lysosomal permeabilization (dashed red line). This causes the release of the lysosomal protease cathepsin B into the cytoplasm which contributes to NLRP3 activation through a yet unknown mechanism. Once activated, NLRP3 initiates cell death and formation of a caspase-1 activating complex termed an “inflammasome”. Processed caspase-1 then cleaves and activates pro-IL-1β, which elicits inflammation upon release from the cell. PYR, pyrin domain; NBD, nucleotide binding domain; LRR, leucine-rich repeats; CARD, caspase recruit domain.
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Comment on

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