The innate immune system is activated by the recognition of antigenic determinants common to a wide spectrum of microbes (the pathogen associated molecular patterns ) and leads to a state of inflammation to alert and combat the ongoing infection ( 33, 34, 38). These anatomical barriers are reinforced by soluble factors (complement system, pentraxins, collectins and the defensins antimicrobial peptides) as well as by leukocytes (macrophages, dendritic cells, mast cells, neutrophils, eosinophils, natural killer cells) that neutralize pathogens or kill the infected cells ( 33, 34). It relies on anatomical barriers (the skin and the mucosa lining the respiratory, gastrointestinal and urogenital tracts) to prevent foreign entities from entering the organism ( 33, 34). The innate immune system, the components of which are already present before any pathogenic intrusion, is fast acting. It eliminates foreign entities (pathogens and toxins) but tolerates the self (host’s own tissues) and its associated microbiota ( 33, 36, 37). The immune system has the unique ability to distinguish self from non-self to protect the host organisms from a plethora of microorganisms and toxins ( 33– 35). Consequently, ROS levels are contributing determinants for various forms of cell death, including apoptosis, necrosis/necroptosis, ferroptosis, pyroptosis and autophagic cell death ( 25– 32). Excessive ROS production plays a major role in the initiation and amplification of cell death by modulating many signaling pathways. Consequently, the cells accumulate oxidative damage within the DNA, lipids and proteins, causing cellular dysfunction and cell death ( 19– 23). The accumulation of ROS can lead to a state of oxidative stress when the endogenous antioxidant machinery of the cell is overwhelmed ( 19– 24). These secondary species are poorly controlled and rapidly and irreversibly react with virtually all classes of biomolecules causing oxidative damage. Interestingly, although even at high concentrations O 2-., NO and H 2O 2 are not directly damaging to cells, they react with themselves or with metal ions to produce the extremely toxic secondary reactive species.OH, ONOO - and HOCl. This can be explained, in part, by the fact that to some extent primary species reactions with biomolecules are reversible and they are easily controlled by enzymatic and non-enzymatic antioxidant molecules of the cell antioxidant machinery ( 15– 18). At low concentrations, which can be handled by the cellular antioxidant system, O 2-., NO and H 2O 2 are necessary for signal transduction, cell migration, cell differentiation, cell proliferation, vasoconstriction, inflammation, senescence and aging ( 4– 14). Interestingly, cellular enzymatic systems such as the nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) oxidases, the myeloperoxidases, the nitric oxide synthases (NOS), the monooxygenase activity of cytochrome P450, xanthine oxidase, monoamine oxidase (MAO) and the mitochondrial respiratory chain are sources of the primary radical species (O 2-., NO, and H 2O 2) ( 1, 3). In contrast, the non-radical products, e.g., hydrogen peroxide (H 2O 2), hypochlorous acid (HOCl), and peroxynitrite (ONOO -), do not have unpaired electrons but remain powerful oxidizing agents ( 1). The radical species, e.g., superoxide anion (O 2-.), hydroxyl radical (.OH), and nitric oxide (NO), have unpaired electrons ( 1, 2). Reactive oxygen species (ROS) include both radical and non-radical species and are formed by the partial reduction of oxygen. We examine how ROS contribute to T-cell biology and discuss whether this activity can be extrapolated to B cells. Here in this mini review, we focus on the role of ROS in adaptive immunity. Reactive oxygen species (ROS) have been implicated in many aspects of the immune responses to pathogens, mostly in innate immune functions, such as the respiratory burst and inflammasome activation. The adaptive immune response calls on T lymphocytes as well as the B lymphocytes essential for the elimination of pathogens and the establishment of the immunological memory. Activation of the innate immune response leads to a state of inflammation that serves to both warn about and combat the ongoing infection and delivers the antigenic information of the invading pathogens to initiate the slower but highly potent and specific second line of defense, the adaptive immune system. It involves anatomical barriers, physiological factors as well as a subset of haematopoietically-derived cells generically call leukocytes. The innate immune system, which is by nature fast acting, represents the first line of defense. To perform this delicate but essential task, the immune system relies on two lines of defense. The immune system protects the host from a plethora of microorganisms and toxins through its unique ability to distinguish self from non-self.
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