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Pro-inflammatory cytokine pathways encompass the network of signaling events initiated by cytokines such as interleukins (ILs), interferons (IFNs), tumor necrosis factors (TNFs), and chemokines, which mediate inflammation and immune cell communication. These pathways regulate leukocyte recruitment, proliferation, differentiation, and inflammatory cell death mechanisms such as pyroptosis, apoptosis, and necroptosis. Dysregulation of these pathways is implicated in the pathogenesis of a wide range of conditions, from infectious diseases and sepsis to cancer, autoimmunity, and chronic inflammatory diseases. Therapeutic agents targeting single cytokines or their receptors have demonstrated efficacy in reducing inflammation, but broad targeting or combined inhibition can lead to high risks of immunosuppression and other safety concerns[1][2][5][6].
Inhibition of cytokine binding to receptor; Blockade of receptor signaling (e.g., JAK/STAT pathway inhibition); Neutralization of circulating cytokines (monoclonal antibodies)
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