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. 2019 Oct 18;7:419. doi: 10.3389/fped.2019.00419

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Copyright © 2019 Tombetti, Giani, Brucato and Cimaz.

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) and the copyright owner(s) 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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Drivers of pericardial inflammation. Autoimmunity against cardiac antigens as well as dysregulated innate immunity might result in pericardial inflammation. Innate immunity is activated by receptors for pathogen- or damage-associated molecular patterns (PAMPs and DAMPs, respectively). Crucial innate immunity pathways leading to pericardial inflammation depend on inflammasome activity and on TNF receptor-1 (TNFR1). The inflammasome is a multimolecular complex composed of sensor protein such as NLRP3 or pyrin (that self-assemble upon activation), stimuli such as NLRP3 or pyrin, adaptor proteins such as ASC, and pro-caspase-1. Upon inflammasome assembly, pro-caspase 1 releases active caspase 1, which can process pro-IL1 to active IL1. AHA: anti-heart antibodies, AIDA: anti-intercalated disc antibodies.