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Inflammatory cytokine signaling refers to the complex network by which pro-inflammatory cytokines—such as interleukin‑1β (IL‑1β), interleukin‑6 (IL‑6), tumor necrosis factor alpha (TNFα), interferon gamma—mediate communication between immune cells during an immune response. These small proteins are secreted primarily by activated macrophages and other leukocytes in response to infection or tissue injury. They bind specific cell-surface receptors on target cells throughout the body, triggering intracellular signal transduction cascades—including MAPK/JNK/p38 pathways—that activate transcription factors like NF-kappaB and STATs. This results in upregulation of genes encoding additional pro-inflammatory mediators and acute-phase proteins. While essential for host defense against pathogens and tissue repair, dysregulated or excessive inflammatory cytokine production can drive chronic inflammation underlying autoimmune diseases, sepsis, cancer progression, neurodegeneration, and other pathologies. Therapeutic strategies often focus on blocking key nodes within these pathways using monoclonal antibodies against individual cytokines/receptors or small-molecule inhibitors targeting downstream kinases.
Monoclonal antibodies neutralizing specific cytokines or their receptors to block downstream inflammatory signals. Small molecules or biologics inhibiting intracellular kinases involved in signal transduction cascades such as JAKs and mTOR. Receptor antagonists preventing ligand binding and activation of pro-inflammatory pathways.
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