PreprintArticleVersion 1Preserved in Portico This version is not peer-reviewed
Redox Regulation of the Immune Response: Nitro-Oxidative Stress and Antioxidants Regulate Macrophage, Neutrophil, and T and B Lymphocyte, and Dendritic and Natural Killer Cell Functions
Version 1
: Received: 7 May 2021 / Approved: 10 May 2021 / Online: 10 May 2021 (11:43:52 CEST)
How to cite:
Morris, G.; Maes, M. Redox Regulation of the Immune Response: Nitro-Oxidative Stress and Antioxidants Regulate Macrophage, Neutrophil, and T and B Lymphocyte, and Dendritic and Natural Killer Cell Functions. Preprints2021, 2021050180. https://doi.org/10.20944/preprints202105.0180.v1
Morris, G.; Maes, M. Redox Regulation of the Immune Response: Nitro-Oxidative Stress and Antioxidants Regulate Macrophage, Neutrophil, and T and B Lymphocyte, and Dendritic and Natural Killer Cell Functions. Preprints 2021, 2021050180. https://doi.org/10.20944/preprints202105.0180.v1
Morris, G.; Maes, M. Redox Regulation of the Immune Response: Nitro-Oxidative Stress and Antioxidants Regulate Macrophage, Neutrophil, and T and B Lymphocyte, and Dendritic and Natural Killer Cell Functions. Preprints2021, 2021050180. https://doi.org/10.20944/preprints202105.0180.v1
APA Style
Morris, G., & Maes, M. (2021). Redox Regulation of the Immune Response: Nitro-Oxidative Stress and Antioxidants Regulate Macrophage, Neutrophil, and T and B Lymphocyte, and Dendritic and Natural Killer Cell Functions. Preprints. https://doi.org/10.20944/preprints202105.0180.v1
Chicago/Turabian Style
Morris, G. and Michael Maes. 2021 "Redox Regulation of the Immune Response: Nitro-Oxidative Stress and Antioxidants Regulate Macrophage, Neutrophil, and T and B Lymphocyte, and Dendritic and Natural Killer Cell Functions" Preprints. https://doi.org/10.20944/preprints202105.0180.v1
Abstract
An immune-inflammatory response is accompanied by increased nitro-oxidative stress. The aims of this mechanistic review are to review: a) the role of redox sensitive transcription factors and enzymes, ROS/RNS production and the activity of cellular antioxidants on the activation and performance of macrophages, dendritic cells, neutrophils, T cells, B cells and natural killer cells; b) the involvement of high-density lipoprotein (HDL), apolipoprotein (Apo)A1, paraoxonase (PON)-1, and oxidized phospholipids in the regulation of the immune response; and c) the detrimental effects of hypernitrosylation and chronic nitro-oxidative stress on the immune response. The redox changes during immune-inflammatory responses are orchestrated by the actions of nuclear factor (NF)-κB, HIF1alpha, the mechanistic target of rapamycin (mTor), the phosphatidylinositol 3‑kinase (PI3K) / protein kinase B (AKT) signalling pathway, mitogen-activated protein (MAP) kinases, 5' AMP-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor (PPAR). The performance and survival of individual immune cells is under redox control and sensitive to intracellular and extracellular levels of ROS/RNS and is heavily influenced by cellular anti-oxidants including the glutathione and thioredoxin systems, nuclear factor erythroid 2-related factor 2 (Nrf-2), and the HDL complex. Chronic nitro-oxidative stress and hypernitrosylation inhibit the activity of those antioxidant systems, the tricarboxylic acid cycle, mitochondrial functions, and the metabolism of immune cells. In conclusion, those redox-associated mechanisms modulate metabolic reprogramming of immune cells, macrophage and T helper cell polarization, phagocytosis, production of pro- versus anti-inflammatory cytokines, immune training and tolerance, chemotaxis, pathogen sensing, antiviral and antibacterial effects, Toll-like receptor activity, and endotoxin tolerance.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
