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Host immune recognition molecules are a broad class of proteins that serve as the primary sensors for the immune system to detect the presence of pathogens or cellular damage. This category includes Pattern Recognition Receptors (PRRs) such as Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-I-like receptors (RLRs), which identify conserved Pathogen-Associated Molecular Patterns (PAMPs) (Janeway & Medzhitov, 2002; Takeuchi & Akira, 2010). Additionally, these molecules recognize Damage-Associated Molecular Patterns (DAMPs) released from stressed or necrotic host cells, thereby initiating sterile inflammatory responses (Kono & Rock, 2008). Major Histocompatibility Complex (MHC) molecules also fall under this umbrella, as they are essential for presenting antigens to T cells, bridging innate and adaptive immunity (Kumar et al., 2011). In therapeutic contexts, these molecules are targeted by agonists to enhance vaccine efficacy or treat cancer, and by antagonists to manage autoimmune and inflammatory disorders (Kawai & Akira, 2011). Due to their fundamental role in immune activation, pharmacological manipulation of these targets carries risks of systemic inflammation or impaired host defense.
Modulation of innate and adaptive immune signaling through the activation or inhibition of receptors that recognize pathogen-associated or damage-associated molecular patterns (Kawai & Akira, 2011; Takeuchi & Akira, 2010).
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