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"Inflammatory cytokines release" refers to the tightly regulated process by which immune cells, such as macrophages, neutrophils, and T cells, secrete small signaling proteins called cytokines into the extracellular environment in response to infection, tissue injury, or immune stimuli. Key cytokines include tumor necrosis factor, interleukins (e.g., IL-1, IL-6), and interferons. These cytokines mediate cell-cell communication to coordinate inflammation, recruit immune cells, and promote host defense. However, excessive or dysregulated cytokine release leads to pathological inflammation and tissue damage, as seen in cytokine release syndrome ("cytokine storm"), sepsis, and autoimmune diseases. Various molecular pathways, such as Toll-like receptor signaling, JAK-STAT, MAPK, and NF-κB, regulate cytokine gene expression and secretion, providing therapeutic targets for immune-mediated diseases[1][2][4][7].
Inhibition of cytokine secretion (via neutralizing antibodies—e.g., anti-TNF, anti-IL-6); Inhibition of cytokine receptors (blocking downstream signaling); Modulation of transcription factors (e.g., NF-κB, STATs) -- which control cytokine gene expression; Inhibition of intracellular signaling pathways (e.g., JAK-STAT, MAPK)
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