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Innate immune sensors and antigen-presenting cells (APCs) represent a broad functional category of the immune system rather than a single molecular target. Innate immune sensors, primarily pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs), STING, and NOD-like receptors (NLRs), detect pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) [1, 4]. APCs, including dendritic cells, macrophages, and B cells, process these signals to initiate and shape adaptive immune responses through antigen presentation and cytokine secretion [2, 5]. In oncology, targeting these sensors (e.g., via STING or TLR agonists) aims to convert "cold" tumors into "hot" tumors by enhancing the recruitment and activation of T cells [3]. Conversely, in autoimmune and inflammatory diseases, inhibiting these pathways can reduce pathological inflammation [4]. Because this term encompasses a wide array of distinct proteins and cell types, it is generally considered a therapeutic area or mechanism of action class rather than a specific drug target [5].
Agonism or antagonism of pattern recognition receptors (PRRs) to modulate innate immune activation and subsequent antigen presentation to the adaptive immune system.
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