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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 8459402, 23 pages
Review Article

Redox Regulation of Inflammatory Processes Is Enzymatically Controlled

1Department of Structural Biology, Institute of Zoology, Kiel University, Kiel, Germany
2Brighton and Sussex Medical School, Falmer, Brighton, UK
3Leibniz-Institute for Plasma Science and Technology (INP Greifswald), ZIK plasmatis, Greifswald, Germany
4Department of Neurology, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany

Correspondence should be addressed to Eva-Maria Hanschmann; ed.frodlesseud-inu.dem@nnamhcsnah.airam-ave

Received 3 March 2017; Revised 6 July 2017; Accepted 25 July 2017; Published 8 October 2017

Academic Editor: Shane Thomas

Copyright © 2017 Inken Lorenzen et al. 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.


Redox regulation depends on the enzymatically controlled production and decay of redox active molecules. NADPH oxidases, superoxide dismutases, nitric oxide synthases, and others produce the redox active molecules superoxide, hydrogen peroxide, nitric oxide, and hydrogen sulfide. These react with target proteins inducing spatiotemporal modifications of cysteine residues within different signaling cascades. Thioredoxin family proteins are key regulators of the redox state of proteins. They regulate the formation and removal of oxidative modifications by specific thiol reduction and oxidation. All of these redox enzymes affect inflammatory processes and the innate and adaptive immune response. Interestingly, this regulation involves different mechanisms in different biological compartments and specialized cell types. The localization and activity of distinct proteins including, for instance, the transcription factor NFκB and the immune mediator HMGB1 are redox-regulated. The transmembrane protein ADAM17 releases proinflammatory mediators, such as TNFα, and is itself regulated by a thiol switch. Moreover, extracellular redox enzymes were shown to modulate the activity and migration behavior of various types of immune cells by acting as cytokines and/or chemokines. Within this review article, we will address the concept of redox signaling and the functions of both redox enzymes and redox active molecules in innate and adaptive immune responses.