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. 2018 Apr 11;9:736. doi: 10.3389/fimmu.2018.00736

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Copyright © 2018 Ağaç, Gill and Farrar.

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 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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ADRB2-mediated suppression of inflammatory processes. Adrenergic signaling through the ADRB2 inhibits various virus-induced immune mediators. [1] Rhinovirus (RV) infects the upper airways by binding to ICAM-1 on the surface of lung ECs. RV infection of ECs upregulates ICAM-1 as well as IL-8, IL-6, CCL5, CCL11, and CXCL10 to recruit inflammatory cells. [2] Activation of the ADRB2 by either the natural ligands epinephrine and norepinephrine or by β2-agonists downregulates ICAM-1 as well as IL-8, CCL5, and GM-CSF from ECs. [3] ADRB2 signaling additionally inhibits pro-inflammatory mediators in innate and adaptive immune cells. Abbreviations: EC, epithelial cell; MC, mast cell; Mɸ, macrophage.