Abstract
Significance: Autoimmune diseases are progressively affecting westernized societies, as the proportion of individuals suffering from autoimmunity is steadily increasing over the past decades. Understanding the role of reactive oxygen species (ROS) in modulation of the immune response in the pathogenesis of autoimmune disorders is of utmost importance. The focus of this review is the regulation of ROS production within tolerogenic dendritic cells (tolDCs) and regulatory T (Treg) cells that have the essential role in the prevention of autoimmune diseases and significant potency in their therapy. Recent Advances: It is now clear that ROS are extremely important for the proper function of both DC and T cells. Antigen processing/presentation and the ability of DC to activate T cells depend upon the ROS availability. Treg differentiation, suppressive function, and stability are profoundly influenced by ROS presence. Critical Issues: Although a plethora of results on the relation between ROS and immune cells exist, it remains unclear whether ROS modulation is a productive way for skewing T cells and DCs toward a tolerogenic phenotype. Also, the possibility of ROS modulation for enhancement of regulatory properties of DC and Treg during their preparation for use in cellular therapy has to be clarified. Future Directions: Studies of DC and T cell redox regulation should allow for the improvement of the therapy of autoimmune diseases. This could be achieved through the direct therapeutic application of ROS modulators in autoimmunity, or indirectly through ROS-dependent enhancement of tolDC and Treg preparation for cell-based immunotherapy. Antioxid. Redox Signal. 34, 364-382.
Highlights
Reactive oxygen species (ROS) are associated with the eradication of invading microorganisms, promotion of inflammation and tissue damage
Multiple organs and tissues are targeted by the autoimmune response in systemic autoimmune disorders, such as systemic lupus erythematosus (SLE), while specific cells and structures of the certain organs are targeted in organ-specific autoimmune diseases, such as insulinproducing β cells of the pancreas in type 1 diabetes (T1D), cartilage of the joints in rheumatoid arthritis (RA), and myelin sheaths and neurons of the brain and spinal cord in multiple sclerosis (MS)
reactive oxygen species (ROS) appear to be crucial for the function of T cells and dendritic cells (DC) acting as signalling molecules involved in the activation and differentiation of these cells
Summary
Reactive oxygen species (ROS) are associated with the eradication of invading microorganisms, promotion of inflammation and tissue damage. One population of CD4+ cells that expresses TCR with high avidity for auto-antigens normally exit the thymus and these are called the Treg cells [104, 175] Their function is to maintain self-tolerance and immune system homeostasis (Fig 2). Contact-dependent inhibition by Treg relies on the expression of CTLA-4, a co-inhibitory molecule that competes with the co-receptor CD28 in binding to the co-stimulatory molecules (CD80 and CD86) on antigen-presenting cells In this way, Treg cells prevent the activation of the pathogenic T cells specific for the same autoantigen and induce tolerogenic properties in DC [177]. ROS production in Treg is explored as a novel mode of Treg suppressive effects
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