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Innate pattern-recognition receptors (PRRs) are a diverse class of germline-encoded host sensors that detect pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) (Janeway & Medzhitov, 2002). This group includes Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), NOD-like receptors (NLRs), and C-type lectin receptors (CLRs), as well as cytosolic DNA sensors like cGAS (Li & Chen, 2018). Upon activation by ligands such as viral vectors or vaccine adjuvants like AS01B, these receptors trigger signaling cascades that lead to the production of pro-inflammatory cytokines and type I interferons (Didierlaurent et al., 2017). This process is crucial for the maturation of antigen-presenting cells and the subsequent orchestration of robust adaptive immune responses. While essential for host defense and vaccine efficacy, dysregulated PRR signaling is implicated in chronic inflammatory and autoimmune disorders (Kawai & Akira, 2010).
Activation of innate immune signaling pathways, such as the MyD88 and TRIF cascades, to induce the expression of pro-inflammatory cytokines and type I interferons, thereby enhancing antigen presentation and adaptive immune activation.
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