先天免疫系统
细胞生物学
促炎细胞因子
TLR4型
模式识别受体
生物
细胞外
炎症
潮湿
受体
过氧化物还原蛋白
信号转导
免疫学
生物化学
酶
过氧化物酶
气象学
物理
作者
Bernard Knoops,Sarah Becker,Mégane A. Poncin,Julien Glibert,Sylvie Derclaye,André Clippe,David Alsteens
标识
DOI:10.1016/j.chembiol.2018.02.006
摘要
Inflammation is a pathophysiological response of innate immunity to infection or tissue damage. This response is among others triggered by factors released by damaged or dying cells, termed damage-associated molecular pattern (DAMP) molecules that act as danger signals. DAMPs interact with pattern recognition receptors (PRRs) to contribute to the induction of inflammation. However, how released peroxiredoxins (PRDXs) are able to activate PRRs, such as Toll-like receptors (TLRs), remains elusive. Here, we used force-distance curve-based atomic force microscopy to investigate the molecular mechanisms by which extracellular human PRDX5 can activate a proinflammatory response. Single-molecule experiments demonstrated that PRDX5 binds to purified TLR4 receptors, on macrophage-differentiated THP-1 cells, and on human TLR4-transfected CHO cells. These findings suggest that extracellular PRDX5 can specifically trigger a proinflammatory response. Moreover, our work also revealed that PRDX5 binding induces a cellular mechanoresponse. Collectively, this study provides insights into the role of extracellular PRDX5 in innate immunity.
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