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Proinflammatory cytokines in the interleukin family (most notably Interleukin-1 alpha, Interleukin-1 beta, Interleukin-18, Interleukin-33, Interleukin-36 subtypes) are small secreted proteins central to the innate and adaptive immune response. They signal through specific cell surface receptors, triggering inflammation, fever, tissue recruitment and proliferation of immune cells, and modulation of pain perception. Dysregulation is implicated in a wide range of diseases spanning infection, autoimmunity, cancer, neurodegeneration, and chronic pain. Therapeutically, these cytokines (or their receptors) are targeted by monoclonal antibodies or antagonists to block excessive inflammation, with notable safety challenges in maintaining immune homeostasis.
Neutralization of cytokine or receptor (e.g., monoclonal antibodies binding IL-1β, blocking its action) Competitive antagonism at the receptor (e.g., IL-1Ra competes with IL-1α/β for IL-1 receptor binding) Down-regulation of cytokine synthesis Blocking signaling pathways (e.g., TIR domain inhibition)
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