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. 2020 Jul 21;11:1318. doi: 10.3389/fimmu.2020.01318

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Copyright © 2020 Vandewalle and Libert.

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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Mechanisms of glucocorticoid resistance (GCR) in sepsis. Pro-inflammatory cytokines and oxidative stress have shown to interfere with the GC signaling pathway at multiple levels. This leads to an inadequate response of the GR to both endogenous (cortisol/corticosterone) and exogenous GCs to tolerate collateral damage induced by sepsis. Vitamin C has been shown to restore the GR function by reverting the effect of oxidative stress on GR's ligand- and DNA-binding capacity. TF-BS, transcription factor binding site; GRE, GC-responsive element; NTL, nuclear translocation.