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Interleukin‑1 beta (IL‑1β), interleukin‑6 (IL‑6), and tumor necrosis factor alpha (TNF–α) are proinflammatory cytokines produced primarily by immune cells such as macrophages and monocytes. They play central roles in mediating the inflammatory response by promoting cell recruitment to sites of injury or infection, inducing fever, stimulating acute phase protein production in the liver, modulating cell proliferation/apoptosis pathways, and influencing neuroimmune interactions. Overproduction or dysregulation of these cytokines is implicated in numerous pathological conditions including autoimmune diseases like rheumatoid arthritis; metabolic disorders such as type II diabetes; neurodegenerative diseases like Alzheimer’s disease; cardiovascular disease; cancer progression via effects on tumor growth/angiogenesis/metastasis; mood disorders such as depression linked to chronic inflammation. Therapeutic agents targeting each individual cytokine have been developed for clinical use—these include monoclonal antibodies or receptor antagonists that block their activity to reduce pathological inflammation but may increase susceptibility to infections due to broad immunosuppressive effects.
Blockade of cytokine-receptor interaction to reduce inflammation and immune activation
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