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. 2019 Aug 9;10:1870. doi: 10.3389/fimmu.2019.01870

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Copyright © 2019 Gruenbacher, Gander, Rahm, Dobler, Drasche, Troppmair, Nussbaumer and Thurnher.

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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Graphical summary: the metabolic reprogramming during macrophage polarization induced by M-CSF (M2) and reinforced by IL-10 (M2c) leads to P2Y₁₁ receptor upregulation. Metabolic reprogramming involves activation of a signaling axis comprising AMP-activated kinase (AMPK), nicotinamide phosphoribosyltransferase (NAMPT), and NAD⁺. NAMPT is the rate-limiting enzyme of the NAD⁺ salvage pathway, which converts nicotinamide (NAM) into nicotinamide mononucleotide (NMN). NAD⁺ acts as macrophage metabolite that drives P2Y₁₁ receptor expression, possibly via the NAD⁺-dependent deactylase SIRT1.