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Interleukin 6 (IL‑6), interleukin 1 beta (IL‑1β), and tumor necrosis factor alpha (TNF‑α) are major proinflammatory cytokines produced primarily by cells involved in innate immunity such as macrophages. They play central roles in regulating immune responses during infection, trauma, or tissue damage by promoting inflammation through complex signaling networks. Each has unique biological properties but also overlapping functions; they stimulate acute phase responses, modulate neuropeptide biosynthesis,[2] regulate cell survival/death decisions,[3] and contribute significantly to the pathogenesis of chronic inflammatory conditions including autoimmune disorders, cardiovascular disease, cancer progression,[4][5] neurodegeneration,[4] sarcopenia/frailty,[4] among others. These molecules are established therapeutic targets for monoclonal antibody therapies aimed at reducing pathological inflammation.[3][4]
Neutralization/blockade of the cytokine itself (e.g., anti-TNF agents bind to TNF-alpha preventing receptor activation)[3] ; Blockade of the corresponding receptor (e.g., anti–IL‑6R agents prevent downstream signaling) ; Downregulation/modulation of inflammatory signaling pathways
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