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Pattern recognition and antigen presentation pathways represent the fundamental mechanisms by which the innate immune system detects threats and initiates adaptive immunity. Dendritic cells (DCs) and other professional antigen-presenting cells (APCs) utilize various Pattern Recognition Receptors (PRRs), including Toll-like receptors (TLRs), NOD-like receptors (NLRs), and C-type lectin receptors (CLRs), to sense pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) (Takeuchi & Akira, 2010, Cell). Following recognition, APCs undergo maturation, characterized by the upregulation of Major Histocompatibility Complex (MHC) molecules and co-stimulatory signals like CD80 and CD86 (Banchereau & Steinman, 1998, Nature). These pathways are essential for the processing of exogenous and endogenous antigens into peptides that are presented to T-cell receptors (TCRs), thereby orchestrating specific immune responses (Roche & Furuta, 2015, Nat Rev Immunol). In clinical practice, these pathways are targeted using PRR agonists as vaccine adjuvants or in cancer immunotherapy to overcome immune tolerance (Kaczanowska et al., 2013, Front Immunol). Conversely, overactivation of these pathways is a hallmark of many autoimmune and inflammatory diseases, making them significant areas of therapeutic research (Kawai & Akira, 2010, Nat Immunol).
Agonism of pattern recognition receptors (PRRs) to stimulate the maturation of dendritic cells and enhance the presentation of antigens to T cells.
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