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Antigen processing and presentation is a critical biological pathway rather than a single molecule, involving the enzymatic degradation of proteins into peptides and their subsequent loading onto Major Histocompatibility Complex (MHC) molecules for display on the cell surface [1][2]. This process is essential for the adaptive immune system to monitor cellular health; MHC Class I molecules present endogenous peptides to CD8+ cytotoxic T cells, while MHC Class II molecules present exogenous peptides to CD4+ helper T cells [2][3]. In the context of oncology, defects in antigen processing—such as the downregulation of the Transporter associated with Antigen Processing (TAP) or MHC subunits—allow tumor cells to evade immune detection [5]. Conversely, in autoimmune diseases, the inappropriate presentation of self-antigens triggers a deleterious immune response against the body's own tissues [1]. Therapeutic intervention often involves targeting specific components of this pathway, such as the proteasome or cathepsins, to modulate immune signaling in cancer and inflammatory conditions [4].
Drugs targeting this pathway typically act by inhibiting the 26S proteasome to prevent the degradation of intracellular proteins into peptides (e.g., Bortezomib), or by modulating the expression of MHC molecules and transporters like TAP to alter the visibility of cells to the immune system [3][4].
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