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. 2022 May 25;13:914033. doi: 10.3389/fimmu.2022.914033

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Copyright © 2022 Weiß, Ramos and Delgobo

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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Treg-mediated effects in myocardial repair and inflammation after infarction. Tregs control local immune responses through a multitude of mechanisms, including inhibiting both canonical T_H1/T_H17 cytokine production and leukocyte migration. Treg cytokines (e.g. IL-10 and TGF-β) and purinergic metabolism products may modulate macrophage polarization towards a pro-healing/reparative phenotype. In addition, Tregs contribute to fibroblast activation and steady collagen deposition in the infarcted area.