Immune-Mediated Toxic Reactions: The Contribution of ROS, Cytokines, and Autoantibodies

dc.contributor.authorZakaria Ali
dc.date.accessioned2026-07-14T12:16:06Z
dc.date.available2026-07-14T12:16:06Z
dc.date.issued2025
dc.description.abstractImmune-mediated toxic reactions represent a significant subset of pathological conditions where dysregulated immune responses contribute directly to tissue damage and organ dysfunction. Central to these reactions are three interrelated mediators: reactive oxygen species (ROS), pro-inflammatory cytokines, and autoantibodies. ROS, generated by activated immune cells, cause oxidative damage to lipids, proteins, and nucleic acids, amplifying inflammatory cascades. Cytokines orchestrate immune cell recruitment and activation, but their excessive or persistent release can exacerbate tissue injury. Autoantibodies, hallmark features of autoimmune conditions, target self-antigens, inducing complement activation, cell lysis, and chronic inflammation. The interplay between ROS, cytokines, and autoantibodies creates a self-perpetuating cycle of immune-mediated toxicity, contributing to the pathogenesis of autoimmune diseases, drug hypersensitivities, and chronic inflammatory conditions. Understanding the mechanistic roles of these mediators provides insight into disease progression and highlights therapeutic targets aimed at modulating oxidative stress, cytokine signaling, and autoantibody production. This review synthesizes current knowledge on the cellular and molecular mechanisms of immune-mediated toxi reactions, emphasizing the integration of redox biology, immunology, and autoimmunity in the development of tissue injury and chronic disease.
dc.description.sponsorshipKampala International University
dc.identifier.issn2992-6122
dc.identifier.urihttp://hdl.handle.net/20.500.12493/14824
dc.language.isoen
dc.publisherNewport International Journal of Biological and Applied Sciences (NIJBAS)
dc.titleImmune-Mediated Toxic Reactions: The Contribution of ROS, Cytokines, and Autoantibodies
dc.typeArticle
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