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Innate immune signaling pathways represent a broad category of molecular networks responsible for the rapid detection of pathogens and cellular stress, rather than a single therapeutic target (NIH, 2019). These pathways are initiated by various pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), NOD-like receptors (NLRs), and the cGAS-STING system, which recognize conserved molecular patterns known as PAMPs and DAMPs (NIH, 2021; Wikipedia, 2024). Upon activation, these sensors trigger complex intracellular cascades involving adaptors like MyD88 and STING, kinases like TBK1, and transcription factors like NF-κB and IRFs, leading to the production of pro-inflammatory cytokines and type I interferons (NIH, 2021). Dysregulation of these pathways is a hallmark of various diseases, including chronic inflammation, autoimmune disorders, and cancer, where they can either promote or inhibit tumor progression (Frontiers in Immunology, 2024; NIH, 2019). Therapeutic strategies involve using agonists to boost immune responses in oncology and infectious diseases, or inhibitors to mitigate excessive inflammation in autoinflammatory conditions (Journal of Microbiology, 2025; MDPI, 2025). However, systemic activation of these pathways carries significant risks, such as cytokine release syndrome and tissue damage (NIH, 2025; Journal of Microbiology, 2025). Understanding the complex crosstalk between these pathways is essential for developing precise immunomodulatory therapies (NIH, 2025).
Agonism of pattern recognition receptors (PRRs) to enhance anti-tumor and antiviral responses; antagonism or inhibition of PRRs and downstream signaling components to suppress hyperinflammation and autoimmune reactions.
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