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. 2021 Feb 19;10(2):313. doi: 10.3390/antiox10020313

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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(1) L.m. infection induces cytosolic mtROS production by complex III of the electron transport chain (ETC) in a Toll-like receptor (TLR)-dependent manner. These cytosolic mtROS covalently link the Iκb kinase (IKK) complex subunit NF-kappa-B essential modulator (NEMO) via disulfide bonds. This covalent linkage of NEMO is crucial for proinflammatory signaling and cytokine secretion. (2) After phagocytosis, Nox2-mediated ROS production is induced and the phagosomal ROS inactivate the cathepsins L and S in a redox-dependent manner. This inhibits excessive proteolysis of engulfed peptides and promotes proper presentation of antigens by major histocompatibility complex (MHC)-class II molecules. (3) mtROS disrupt the interaction of thioredoxin-interacting protein (TXNIP) with thioredoxin, enabling its interaction with inflammasome subunit NLRP3. This step is crucial for assembly of the NRLP3 inflammasome and subsequent caspase-1 activation and cleavage of IL-1β and IL-18.