Redox control of NLRP3 inflammasome activation in health and disease

Journal of Leukocyte Biology

Anna Rubartelli¹ 

[1]Cell Biology Unit, IRCCS AOU San Martino, IST Istituto Nazionale per la Ricerca sul Cancro, Genova, ItalyCell Biology Unit, IRCCS AOU San Martino, IST Istituto Nazionale per la Ricerca sul Cancro, Genova, ItalyCell Biology Unit, IRCCS AOU San Martino, IST Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy

关键词: caspase-1;    IL-1β;    IL-1 receptor antagonist;    leaderless secretion;    oxidative stress;    ROS;    antioxidants;   

DOI  :  10.1189/jlb.0512265

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

Shifts in the redox balance between ROS and antioxidants regulate innate immunity at various levels. Changes in the redox microenvironment modulate the activation potential of the NLRP3 inflammasome, a signaling platform that activates caspase-1, allowing the maturation of IL-1β. However, a clear definition of the underlying mechanism is missing. In this essay, I review the most-credited theories on inflammasome activation. In particular, I will focus on the redox-mediated mechanisms that regulate the assembly of NLRP3 inflammasome and discuss how aberrations in them are implicated in the pathogenesis of autoinflammatory diseases.

【 授权许可】

Unknown