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Toll-like receptor 7 (TLR7) and Toll-like receptor 9 (TLR9) are endosomal pattern recognition receptors that play a critical role in the innate immune system by sensing nucleic acids [1, 5]. TLR7 specifically recognizes single-stranded RNA (ssRNA), while TLR9 detects unmethylated CpG DNA motifs, both typically associated with viral and bacterial pathogens [1, 2]. Upon activation, these receptors recruit the adapter protein MyD88, triggering a signaling cascade that results in the production of Type I interferons and pro-inflammatory cytokines such as TNF-alpha and IL-6 [1, 2]. In the context of autoimmune diseases like systemic lupus erythematosus (SLE), the aberrant recognition of self-derived nucleic acids by TLR7 and TLR9 drives chronic inflammation and tissue damage [2, 4]. Therapeutic strategies include the development of dual TLR7/9 antagonists to suppress this overactive immune response in autoimmunity, as well as the use of agonists to stimulate immune activity in oncology and infectious disease settings [3, 4].
TLR7 and TLR9 are endosomal receptors that signal via the MyD88 adapter protein to activate NF-κB and IRF7, leading to the production of pro-inflammatory cytokines and Type I interferons. Antagonists inhibit this signaling to treat autoimmunity, while agonists stimulate it for antiviral or antineoplastic effects.
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