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Antigen-presenting cell activation via tumor-associated antigens refers to the capture, processing, and presentation of tumor antigens by professional APCs—primarily dendritic cells—on MHC class I and II molecules to prime CD8+ and CD4+ T-cell responses against cancer[7][3]. Tumor antigens are commonly categorized as tumor-associated antigens (self-antigens overexpressed or aberrantly expressed in tumors) and tumor-specific antigens (neoantigens unique to tumor cells), both of which can be displayed to T cells, although TAAs carry a risk of off-tumor recognition[6][2][4]. Effective APC activation can be enhanced by innate stimuli (e.g., TLR agonists), DAMPs released during immunogenic cell death, and optimized cross-presentation pathways, while tumors counteract this pathway by reducing antigen expression, impairing MHC-I/HLA-I surface display, or disrupting antigen processing components like TAP and proteasomes[3][7][9]. Although vital for immunotherapy success, this entry is a process-level concept and not a discrete molecular target or receptor.
Enhance dendritic cell maturation and antigen uptake via PRR/TLR stimulation, improving MHC-I cross-presentation and MHC-II presentation of tumor antigens. Increase release of DAMPs and tumor antigens via immunogenic cell death to promote APC activation and T-cell priming. Overcome tumor-mediated downregulation or defects in antigen presentation machinery (e.g., MHC-I/TAP pathway) to restore antigen display to T cells. Provide exogenous tumor antigens (TAAs/TSAs) in vaccine formats to load APCs for T-cell priming.
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