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. 2022 May 2;23(9):5056. doi: 10.3390/ijms23095056

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© 2022 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 (https://creativecommons.org/licenses/by/4.0/).

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The picture represents the effect of A2A receptor activation on NLRP3 inflammasome function in macrophage (A) and microglia (B). (A) In macrophages, adenosine, increased during tissue injury, activates A2A receptor that through cAMP/PKA/CREB/HIF-1α signaling results in upregulation of NLRP3, Caspase-1, and IL1β/IL-18 production. (B) In microglia, adenosine, through A2A receptor, affects NLRP3 inflammasome and caffeine, and by blocking this signal may improve cognition. β-amyloid may engage the NLRP3 inflammasome, promoting production of proinflammatory cytokines.