Abstract
Interleukin-1β (IL-1β) plays a central role in stimulation of innate immune system and inflammation and in several chronic inflammatory diseases. These include rare hereditary conditions, e.g., auto-inflammatory syndromes, as well as common pathologies, such as type II diabetes, gout and atherosclerosis. A better understanding of IL-1β synthesis and release is particularly relevant for the design of novel anti-inflammatory drugs. One of the molecules mainly involved in IL-1β maturation is the P2X7 receptor (P2X7R), an ATP-gated ion channel that chiefly acts through the recruitment of the NLRP3 inflammasome-caspase-1 complex. In this review, we will summarize evidence supporting the key role of the P2X7R in IL-1β production, with special emphasis on the mechanism of release, a process that is still a matter of controversy. Four different models have been proposed: (i) exocytosis via secretory lysosomes, (ii) microvesicles shedding from plasma membrane, (iii) release of exosomes, and (iv) passive efflux across a leaky plasma membrane during pyroptotic cell death. All these models involve the P2X7R.
Highlights
Reviewed by: Robson Coutinho-Silva, Federal University of Rio de Janeiro, Brazil Tobias Engel, Royal College of Surgeons in Ireland, Ireland
One of the molecules mainly involved in IL-1β maturation is the P2X7 receptor (P2X7R), an ATP-gated ion channel that acts through the recruitment of the NLRP3 inflammasome-caspase-1 complex
Its remarkable efficiency and plasticity as an alarm signal strongly depends on the diverse of ATP-selective plasma membrane receptors expressed by immune cells
Summary
Reviewed by: Robson Coutinho-Silva, Federal University of Rio de Janeiro, Brazil Tobias Engel, Royal College of Surgeons in Ireland, Ireland. Extracellular ATP acts at plasma membrane purinergic P2 receptors, the P2X7 receptor (P2X7R) subtype, to drive NLRP3 inflammasome activation and IL-1β processing and release (Ferrari et al, 1997).
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
