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Received Jul 20, 2017; Revised Oct 16, 2017; Accepted Nov 27, 2017
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1. Introduction
Immunosenescence is characterized by age-associated changes in cell phenotype and function that ultimately leads to a general impairment of the immune response [1]. In the innate compartment, in mice as well as in humans, a decrease in neutrophil chemotaxis, phagocytosis, and oxidative burst has been observed along with a decrease in natural killer (NK) cells and macrophage cell functions [2, 3]. Changes in the acquired immunity during ageing are driven by the thymic involution, leading to a decreased production of naïve T cells capable of replenishing the peripheral pool [4]. Furthermore, homeostatic mechanisms as well as persistent infections (i.e., cytomegalovirus) push memory T cells towards several rounds of replication during the ageing process [5–7]. Once reached the replicative senescence, these cells show energy, resistance to apoptosis, and changes in cytokine production [8]. Moreover, the impairment of the immune function during the ageing process can be even promoted by its inability to restore a proper balance between prooxidant, such as reactive oxygen species (ROS), and antioxidant molecules, such as the enzymes superoxide dismutase and catalase or the reducing agent glutathione (GSH). This condition is commonly defined as oxidative stress [9, 10]. ROS are continuously produced in the mitochondria as a result of the reduction of a small percentage of molecular oxygen by leaked electrons in the electron transporting chain or are produced enzymatically by the NADPH oxidase, mediating the respiratory burst in phagocytes. Other sources of ROS include the xanthine oxidase or the nitric oxide synthase pathways as well as environmental ultraviolet or ionizing radiation [11]. ROS play an important role in the immune system other than the respiratory burst, participating in the T, B, NK, and dendritic cell signaling or coordinating the cytokine production [12–14]. Nevertheless, ROS mediate detrimental effects to different cellular components if not properly counterbalanced by the antioxidant system within the cell. Such effects include lipid peroxidation, DNA oxidative damage, and protein modifications like glutathionylation and carbonylation [15, 16]. As an example, in the immune system, it has...