Abstract
Accumulated reactive oxygen species (ROS) directly contribute to biomacromolecule damage and influence various inflammatory responses. Reactive oxygen species act as mediator between innate and adaptive immune cells, thereby influencing the antigen-presenting process that results in T cell activation. Evidence from patients with chronic granulomatous disease and mouse models support the function of ROS in preventing abnormal autoimmunity; for example, by supporting maintenance of macrophage efferocytosis and T helper 1/T helper 2 and T helper 17/ regulatory T cell balance. The failure of many anti-oxidation treatments indicates that ROS cannot be considered entirely harmful. Indeed, enhancement of ROS may sometimes be required. In a mouse model of rheumatoid arthritis (RA), absence of NOX2-derived ROS led to higher prevalence and more severe symptoms. In patients with RA, naïve CD4+ T cells exhibit inhibited glycolysis and enhanced pentose phosphate pathway (PPP) activity, leading to ROS exhaustion. In this “reductive” state, CD4+ T cell immune homeostasis is disrupted, triggering joint destruction, together with oxidative stress in the synovium.
Highlights
Oxidative stress represents an imbalance between pro- and anti-oxidants, in favor of the former, and has generally been considered as potentially harmful, since it leads to phenomena including DNA damage, protein oxidation, and lipid peroxidation [1]
A typical example of this change in research direction is illustrated by the fact that tissuespecific redox modification of proteins has replaced biomacromolecule damage as the main agent involved in the process of aging
Evidence from NOX2-deficient mice and patients with Chronic granulomatous disease (CGD) support the functions of reactive oxygen species (ROS) in regulating T helper 1 (Th1)/T helper 2 (Th2) and T helper 17 (Th17)/Treg balance
Summary
Oxidative stress represents an imbalance between pro- and anti-oxidants, in favor of the former, and has generally been considered as potentially harmful, since it leads to phenomena including DNA damage, protein oxidation, and lipid peroxidation [1]. In contrast to function of preventing excessive antigen reduction characterized in previous section, NOX2-derived ROS in the degradation of apoptotic cells seems to be a positive correlation: efferosomes maturation (acquisition of LC3 and LAMP-1), enhanced acidic environment mediated by V-ATPases, competent proteolytic activity, and these are obviously delayed in macrophage of CGD patients.
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