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Non-specific immune system activation via DAMP-mediated antigen presentation is a complex physiological process rather than a single molecular target. It involves the release of endogenous Damage-Associated Molecular Patterns (DAMPs)—such as HMGB1, calreticulin, and ATP—from cells undergoing stress or immunogenic cell death (Garg et al., 2015). These molecules function as 'danger signals' that are recognized by pattern recognition receptors (PRRs) like Toll-like receptors (TLRs) on innate immune cells (Roh & Sohn, 2018). This recognition stimulates the maturation of dendritic cells and the efficient presentation of cellular antigens to the adaptive immune system, particularly CD8+ T cells (Kroemer et al., 2013). In clinical practice, this mechanism is primarily exploited in oncology, where certain chemotherapies and radiotherapy induce immunogenic cell death to convert the tumor into an 'in situ' vaccine (Galluzzi et al., 2017). However, dysregulation of this pathway can lead to pathological sterile inflammation and autoimmune disorders.
Induction of immunogenic cell death (ICD) which triggers the release of damage-associated molecular patterns (DAMPs) that bind to pattern recognition receptors on dendritic cells, promoting antigen cross-presentation to T cells.
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