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. 2017 Oct 12;8:1257. doi: 10.3389/fimmu.2017.01257

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Copyright © 2017 Moreira-Souza, Almeida-da-Silva, Rangel, Rocha, Bellio, Zamboni, Vommaro and Coutinho-Silva.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed mechanism of T. gondi infection control mediated by extracellular ATP (eATP)/P2X7 receptor and IL-1β, in macrophages. Binding of eATP to the P2X7 receptor may lead to pathogen elimination via different mechanisms: the fusion of lysosomes to the parasitophorous vacuole (forming a phagolysosome), reactive oxygen species (ROS) generation and the activation of the canonical NLRP3 inflammasome. NLRP3 inflammasome activation by eATP potentiates IL-1β release through caspase-1 activity and, in turn, IL-1β in the extracellular compartment binds to its receptor, triggering T. gondii elimination via mitochondrial ROS generation.