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Immune response regulation via anti-inflammatory signaling refers to the biological processes and molecular pathways by which the immune system downregulates inflammation to prevent tissue damage and facilitate recovery[7][3][4]. This regulation is achieved through specific anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β), as well as suppressors of cytokine signaling (SOCS proteins)[2][3]. Anti-inflammatory signaling counterbalances pro-inflammatory mechanisms, resolving acute inflammation, promoting tissue healing, and protecting against autoimmune responses. These mechanisms involve inhibition of key pro-inflammatory pathways like NF-κB, MAPK, and JAK-STAT and are critical for maintaining immune homeostasis[1][3][4]. Dysfunction or dysregulation can lead to chronic inflammatory diseases, impaired host defense against infection, or excessive immunosuppression[7][4].
Enhancement of anti-inflammatory cytokines (e.g., IL-10, TGF-β); Inhibition of pro-inflammatory pathways (e.g., NF-κB, MAPK, JAK-STAT); Blockade of inflammatory mediators (e.g., TNF-α, IL-1β); Induction of suppressors of cytokine signaling (SOCS proteins)
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