Abstract
In the skin, adenosine triphosphate (ATP) is released from various types of cells by various environmental stimuli via nonlytic mechanisms, cell damage, or acute cell death. Because ATP is a potent inducer of skin inflammation, it has to be promptly hydrolyzed for the skin to achieve homeostasis. Of note, ATP activates mast cells (MCs) through P2X7R, leading to the enhanced skin inflammation. However, MC involvement in the impairment of skin inflammation via ATP hydrolysis remains largely unknown.
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