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. 2020 Sep 10;7:537. doi: 10.3389/fmed.2020.00537

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Copyright © 2020 Berry, Haack, Theberge, Brighenti and Svensson.

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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The exchange of soluble factors through paracrine signaling generates context-dependent effects. The secretion of proinflammatory factor IFNγ by T cells induces antimicrobial functions (e.g., autophagy) and signaling (e.g., HIF1α-mediated NO production) in M. tuberculosis-infected macrophages, while increasing the virulence of P. aeruginosa through OprF-binding and downstream induction of virulence factor PA-I. The secretion of IFNγ is decreased by interaction with C. neoformans virulence factor GXM, which decreases secretion of inflammatory factors (TNFα) while increasing secretion of anti-inflammatory factors IL-4 and IL-10. OprF, outer membrane porin F; PA-I, type I P. aeruginosa lectin; HIF1α, hypoxia inducible factor-1 α; NO, nitric oxide; GXM, glucuronoxylomannan.