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Dendritic cell activation and antigen presentation refers to the coordinated processes by which dendritic cells (professional antigen-presenting cells) recognize danger signals, internalize antigens, undergo maturation, migrate to lymphoid organs, and present peptides to T cells via MHC II (to CD4 T cells) and MHC I, including cross-presentation (to CD8 T cells). Activation increases costimulatory molecules and CCR7 and enables priming of naïve T cells, while specialized intracellular trafficking controls peptide loading: MHC II molecules are chaperoned by invariant chain, process CLIP exchange via HLA‑DM, and their ubiquitination and routing change upon activation; cross-presentation uses vacuolar and endosome‑to‑cytosol pathways whose relative in vivo importance varies. DC maturation can create a time-limited “snapshot” of antigens presented and, if preactivated, can impair subsequent MHC II presentation of new antigens. These mechanisms are central to host defense, tolerance, and cancer immunity, and are therapeutically leveraged or impacted by adjuvants, vaccines, and checkpoint blockade.
Pattern-recognition receptor stimulation (e.g., TLR ligands) triggers DC activation/maturation, upregulating costimulation and altering antigen-processing pathways. For MHC II: internalized antigens are degraded in endo/lysosomes; newly synthesized MHC II associates with invariant chain (Ii), CLIP is exchanged for peptides by HLA‑DM; activation blocks MHC II ubiquitination to increase surface presentation. For cross-presentation (MHC I): internalized antigens access MHC I via vacuolar or endosome‑to‑cytosol pathways; DC activation can modulate these pathways. Mature DCs transiently upregulate then shut off new MHC II synthesis, shaping a “snapshot” of antigen presentation; preactivation can impair subsequent MHC II presentation of newly encountered antigens.
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