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Pattern-recognition receptors (PRRs) and antigen receptors are the fundamental sensors of the immune system, responsible for detecting foreign pathogens and endogenous cellular stress. PRRs, including Toll-like receptors (TLRs) and NOD-like receptors (NLRs), recognize conserved molecular patterns to trigger immediate innate immune responses and inflammation (Takeuchi & Akira, 2010). Antigen receptors, specifically B-cell receptors (BCRs) and T-cell receptors (TCRs), undergo genetic rearrangement to provide highly specific recognition of unique epitopes, forming the basis of adaptive immunity (Janeway et al., 2002). These receptors are major therapeutic targets in oncology, infectious diseases, and autoimmune disorders, where they are modulated to either enhance or suppress immune activity (Kanzler et al., 2007). For example, TLR agonists serve as potent vaccine adjuvants, while BCR signaling inhibitors are used to treat B-cell malignancies (O'Neill et al., 2009). Due to their central role in immune homeostasis, pharmacological intervention must be carefully balanced to avoid systemic toxicity or autoimmunity (Kumar et al., 2011).
Agonism or antagonism of innate pattern-recognition receptors or adaptive antigen receptors to modulate immune signaling cascades and cellular activation.
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