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Inflammatory factor regulation refers to a broad biological process rather than a specific molecular target or receptor. It encompasses the intricate networks and feedback mechanisms that control the synthesis, release, and activity of mediators such as cytokines, chemokines, and lipid-derived factors that drive or resolve the immune response [3, 9, 11]. Central to this regulation are master signaling pathways, including the Nuclear Factor-kappa B (NF-κB) and Janus kinase-signal transducer and activator of transcription (JAK-STAT) systems, which integrate physiological signals to modulate gene transcription [5, 9, 10]. Chronic dysregulation of these factors is a fundamental driver in the pathogenesis of autoimmune diseases, chronic inflammatory conditions, and acute systemic crises like sepsis or cytokine release syndrome [1, 9]. Consequently, therapeutic strategies for inflammatory factor regulation utilize a wide array of agents, including corticosteroids and targeted biologics (e.g., TNF-α or IL-6 inhibitors), which aim to restore immune homeostasis and prevent irreversible tissue damage [3, 8, 11].
Modulation of the expression, secretion, and signaling of various pro-inflammatory and anti-inflammatory cytokines and chemokines to restore physiological immune balance and mitigate tissue injury.
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