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. 2019 Jun 6;20(11):2778. doi: 10.3390/ijms20112778

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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P2X7R-mediated NLPR3 inflammasome activation. (A) NLRP3 is composed by an N-terminal pyrin domain (PYD), a central nucleotide-binding-and-oligomerization (NATCH) domain, and a C-terminal leucine-rich repeats (LRR) domain. PYD domain recruits the apoptosis-associated speck-like protein (ASC) that contains a caspase recruitment domain (CARD). This complex recruits the procaspase-1. Together, these components constitute the NLRP3 inflammasome. (B) 1. High ATP levels released from neurons or astrocytes reach P2X7R located in microglia; 2. P2X7R stimulation elicits K⁺ efflux, which may trigger NLRP3 inflammasome assembly and activation through NIMA-related serine/threonine kinase 7 (Nek7) binding; 3. NLRP3 inflammasome mediates the activation of caspase-1; 4. Caspase-1 induces the maturation of interleukins (IL) by cleaving pro-IL-1β and pro-IL-18 in IL-1β and IL-18, respectively; 5. Finally, the mature form of cytokines are secreted.

P2X7R-mediated NLPR3 inflammasome activation. (A) NLRP3 is composed by an N-terminal pyrin domain (PYD), a central nucleotide-binding-and-oligomerization (NATCH) domain, and a C-terminal leucine-rich repeats (LRR) domain. PYD domain recruits the apoptosis-associated speck-like protein (ASC) that contains a caspase recruitment domain (CARD). This complex recruits the procaspase-1. Together, these components constitute the NLRP3 inflammasome. (B) 1. High ATP levels released from neurons or astrocytes reach P2X7R located in microglia; 2. P2X7R stimulation elicits K⁺ efflux, which may trigger NLRP3 inflammasome assembly and activation through NIMA-related serine/threonine kinase 7 (Nek7) binding; 3. NLRP3 inflammasome mediates the activation of caspase-1; 4. Caspase-1 induces the maturation of interleukins (IL) by cleaving pro-IL-1β and pro-IL-18 in IL-1β and IL-18, respectively; 5. Finally, the mature form of cytokines are secreted.