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Chemokine and cytokine induction is a fundamental biological process rather than a discrete molecular target. It involves the coordinated expression and secretion of signaling proteins—cytokines (e.g., interleukins, interferons) and chemokines (e.g., CXCL10, CCL2)—that orchestrate the innate and adaptive immune responses [1][2]. This process is typically initiated by the activation of pattern recognition receptors (PRRs) like Toll-like receptors (TLRs) or the cGAS-STING pathway in response to pathogen-associated or damage-associated molecular patterns [3]. In oncology, the therapeutic induction of these mediators aims to convert immunologically 'cold' tumors into 'hot' tumors by promoting the recruitment and activation of cytotoxic T cells and dendritic cells [4]. Conversely, excessive or uncontrolled induction can lead to life-threatening conditions such as cytokine storms or chronic inflammatory diseases, making this process a critical pharmacodynamic endpoint for both immunostimulatory and immunosuppressive drug development [5]. [1] https://www.nature.com/articles/nri.2017.111 [2] https://www.ncbi.nlm.nih.gov/books/NBK544228/ [3] https://www.frontiersin.org/articles/10.3389/fimmu.2020.01526/full [4] https://www.jci.org/articles/view/120846 [5] https://www.nejm.org/doi/full/10.1056/NEJMra2026131
Activation of pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs), STING, or RLRs to trigger transcriptional programs (e.g., NF-κB, IRF3/7) that lead to the synthesis and secretion of immune signaling proteins.
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