The Selenoprotein MsrB1 Instructs Dendritic Cells to Induce T-Helper 1 Immune Responses
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The Selenoprotein MsrB1 Instructs Dendritic Cells to Induce T-Helper 1 Immune Responses
Ho-Jae Lee, Joon Seok Park, Hyun Jung Yoo, Hae Min Lee, Byung Cheon Lee, and Ji Hyung Kim
Antioxidants
October 20, 2020
Reduction–oxidation (Redox) reactions are important biological reactions that participate in diverse physiological processes throughout the body. One particular Redox reaction is protein oxidation, which is performed by reactive oxygen species (ROS), and is of vital importance in regulating cellular signal transduction, metabolism, and protein activity.
There are a select few sulfur-containing amino acids, methionine (Met) and cysteine (Cys), along with an analog amino acid called selenocysteine (Sec), upon which many oxidative modification processes occur. With Met, oxidation of its sulfur group generates S- and R- stereoisomers of methionine sulfoxide. This can be countered by methionine sulfoxide reductase A (MsrA) and B (MsrB) which, respectively, reduce methionine-S-sulfoxide and methionine-R-sulfoxide (Met-R-SO) back to Met.
In mammals, there are three distinct MsrB proteins: MsrB1, MsrB2, and MsrB3. All can reduce Met-R-SO back to Met. However, unlike MsrB2 and MsrB3, MsrB1 is a selenoprotein, or a protein containing Sec residues that catalyze Redox reactions. MsrB1 further differs from Msrb2 and Msrb3 in that it is mainly expressed in the cytosol and nucleus, where MsrB2 and MsrB3 are only found in the mitochondria and endoplasmic reticulum.
ROS also participate in many immune processes, sometimes by inducing protein oxidation. One well-studied example of the roles of ROS in the innate immune system relates to macrophages and dendritic cells (DCs); When these cells receive signals through pattern recognition receptors, they upregulate their mitochondrial respiration and generate mitochondrial ROS, killing the microbes along with cellular ROS generated by membrane-bound nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complexes. There is also evidence that ROS participate in the ability of innate immune cells to regulate adaptive immune cell functions. Cellular ROS produced by antigen-stimulated DCs regulate the pH in their phagosomes, shaping their antigen presentation and their ability to stimulate T-cell proliferation and cytokine production. Unfortunately, the exact mechanism(s) by which ROS mediate immune cell signaling and how these mechanisms are regulated are still not fully understood.
In this study, researchers demonstrated that MsrB1 plays a vital role in the ability of dendritic cells (DCs) to provide the antigen presentation and co-stimulation needed for cluster of differentiation antigen four (CD4) T-cell priming in mice. Results indicated that MsrB1 regulated signal transducer and activator of transcription-6 (STAT6) phosphorylation in DCs. Further, both in vitro and in vivo, MsrB1 potentiated the lipopolysaccharide (LPS)-induced Interleukin-12 (IL-12) production by DCs and drove T-helper 1 (Th1) differentiation after immunization. This suggests that MsrB1 activates the STAT6 pathway in DCs, inducing DC maturation and IL-12 production that promotes Th1 differentiation.
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