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©The Author(s) 2022.
World J Gastroenterol. Sep 28, 2022; 28(36): 5265-5279
Published online Sep 28, 2022. doi: 10.3748/wjg.v28.i36.5265
Published online Sep 28, 2022. doi: 10.3748/wjg.v28.i36.5265
Figure 1 The activation of the P2X7 receptor and NLRP3 inflammasome.
The P2X7 receptor is activated by extracellular ATP and NAD+ and serves as an ion channel. It can also form non-selective macropores. The activated P2X7 receptor induces the decreasing of intracellular K+, which initiates NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation. The activated process of pro-interleukin (IL)-1β and pro-IL-18 are triggered by the active caspase-1 that results from the formation of NLRP3 inflammasome. Mature inflammatory cytokines are released into extracellular space from cells, which finally results in the cell death. ADPR: ADP-ribose; ARTC2.2: ADP-ribosyltransferase 2.2; ASC: Apoptosis-associated speck-like protein containing a CARD; NLRP3: NOD-like receptor family pyrin domain containing 3; IL-18: Interleukin-18; IL-1β: Interleukin-1β.
- Citation: Jiang ZF, Wu W, Hu HB, Li ZY, Zhong M, Zhang L. P2X7 receptor as the regulator of T-cell function in intestinal barrier disruption. World J Gastroenterol 2022; 28(36): 5265-5279
- URL: https://www.wjgnet.com/1007-9327/full/v28/i36/5265.htm
- DOI: https://dx.doi.org/10.3748/wjg.v28.i36.5265