Immune-inflammatory pathways

Immune-inflammatory pathways represent a sophisticated network of molecular cascades, including the NF-κB, JAK-STAT, and MAPK pathways, which orchestrate the body's response to infection, injury, or cellular stress [6, 8, 15]. These pathways are initiated by the activation of pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs), leading to the production of pro-inflammatory cytokines like TNF-α, IL-1, and IL-6 [9, 13, 16, 17]. While acute activation is essential for host defense and tissue repair, chronic dysregulation is a central driver in the pathogenesis of various conditions, including rheumatoid arthritis, inflammatory bowel disease, and neurodegenerative disorders [1, 6, 7, 15]. Therapeutic strategies focus on modulating specific nodes within these pathways using agents such as monoclonal antibodies that neutralize cytokines, small molecule kinase inhibitors like JAK inhibitors, and traditional anti-inflammatories like corticosteroids [1, 11, 15, 20]. However, systemic inhibition of these pathways often poses significant safety challenges, notably an increased risk of opportunistic infections and malignancy due to broader immunosuppression [1, 11, 21].

Other names

Inflammatory signaling pathwayImmune-mediated pathwayInflammatory cascadePro-inflammatory pathwayImmune-inflammatory cascade

Modulation of pro-inflammatory cytokine signaling, inhibition of intracellular signaling kinases (e.g., Janus kinases, MAP kinases), and suppression of inflammatory transcription factor activation (e.g., NF-κB).