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The term "immune system pathways involved in inflammation" encompasses a range of interconnected cellular signal transduction networks, including those triggered by pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs), which recognize pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs).[4][5][6] Downstream signaling activates transcription factors (e.g., NF-κB, IRF-3/7, AP-1), promoting the production of pro-inflammatory and anti-inflammatory cytokines, chemokines, and growth factors that shape cellular recruitment, activation, and tissue repair.[3][4][5][6] Dysregulation of these pathways contributes to pathological inflammation, including autoimmune diseases, infection, cancer, cardiovascular, and neurodegenerative disorders.[6][7] Because this term refers to a collection of mechanisms rather than a single target, it is not correct to use it as a drug target without further specification. For structured information and drug development, reference should be made to **individual molecules** (e.g., "Tumor necrosis factor-alpha receptor," "Interleukin-6 receptor," "Toll-like receptor 4," etc.), each with specific roles and classification[3][4][5][6][7].
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