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Host immune signaling refers to the integrated network of molecular pathways that detect and respond to pathogens, cellular stress, and tissue damage (Janeway et al., 2001). This broad category includes innate immune mechanisms, such as pattern recognition receptor (PRR) signaling (e.g., Toll-like receptors, STING), and adaptive immune responses involving T-cell and B-cell receptor signaling (Akira et al., 2006). These pathways coordinate the production of cytokines, chemokines, and interferons to eliminate threats and maintain homeostasis (Newton & Dixit, 2012). Dysregulation of host immune signaling is central to the pathogenesis of various conditions, including chronic inflammatory diseases, autoimmune disorders, and the evasion of immune surveillance by tumors (O'Shea et al., 2013). Consequently, many therapeutic interventions target specific nodes within these signaling cascades to either dampen overactive responses or stimulate anti-tumor immunity. However, because "host immune signaling" describes a collection of processes rather than a single protein or receptor, it is classified as a therapeutic area or biological process rather than a discrete molecular target.
Modulation of host immune responses through the inhibition or activation of specific signaling nodes, such as cytokine receptors, intracellular kinases, or immune checkpoints.
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