NCF4 regulates antigen presentation of cysteine peptides by intracellular oxidative response and restricts activation of autoreactive and arthritogenic T cells

• DOI: 10.1016/j.redox.2024.103132
• Publication Date: 2024-03-26T15:52:53Z
• Authors: Jing Xu; Chang He; Yongsong Cai; Xipeng Wang; Jidong Yan; Jing Zhang; Fujun Zhang; Vilma Urbonaviciute; Yuanyuan Cheng; Shemin Lu; Rikard Holmdahl
• Keywords: 0301 basic medicine; Medicine (General); QH301-705.5; T-Lymphocytes; Lymphocyte Activation; Arthritis, Rheumatoid; Mice; 03 medical and health sciences; R5-920; Neutrophil cytosolic factor 4 (NCF4, earlier often denoted p40phox); Animals; Cysteine; Biology (General); Antigen presentation; Neutrophil cytosolic factor 1 (NCF1, earlier often denoted p47phox); Intracellular reactive oxygen species; Antigen Presentation; T cell activation; Macrophages; NADPH Oxidases; Redox regulation; Reactive Oxygen Species; Peptides; Oxidation-Reduction; Research Paper

Autoimmune diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematous, are regulated by polymorphisms in genes contributing to the NOX2 complex. Mutations both Ncf1 Ncf4 affect development of experimental models RA, but different regulatory pathways mediated NOX2-derived reactive oxygen species (ROS) have not yet been clarified. Here we address possibility that intracellular ROS, NCF4 protein (earlier often denoted p40phox) which interacts with endosomal membranes, could play an important role oxidation cysteine peptides mononuclear phagocytic cells, thereby regulating antigen presentation activation arthritogenic T cells. To study used mice amino acid replacing mutation (NCF4