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Toll-like receptor 7 (TLR7) is a key pattern recognition receptor (PRR) of the innate immune system, primarily localized in the endosomes of plasmacytoid dendritic cells (pDCs) and B cells [1, 9]. It specializes in detecting single-stranded RNA (ssRNA) from viruses and bacteria, as well as endogenous RNA in certain pathological states [2, 12]. Upon ligand binding, TLR7 initiates a MyD88-dependent signaling pathway that leads to the production of type I interferons (IFN-α/β) and pro-inflammatory cytokines like IL-6 and TNF-α [6, 13]. This response is vital for antiviral defense and can be harnessed for cancer immunotherapy, where TLR7 agonists like imiquimod are used to stimulate antitumor immunity [4, 7]. However, overactivation of TLR7 by self-nucleic acids is strongly linked to the development of autoimmune diseases, most notably systemic lupus erythematosus (SLE) [2, 15]. As a result, TLR7 is a dual-purpose therapeutic target: agonists are developed for infectious diseases and oncology, while antagonists are investigated for managing chronic inflammatory and autoimmune conditions [9, 11].
Agonism of the MyD88-dependent signaling pathway to induce type I interferons and pro-inflammatory cytokines for antiviral and antineoplastic effects; Antagonism to inhibit aberrant immune activation in autoimmune disorders [2, 6, 9].
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