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Inflammatory gene expression pathways comprise a broad collection of signaling pathways and gene networks activated during tissue injury, infection, or immune responses, resulting in the upregulation or downregulation of genes related to cytokines, chemokines, adhesion molecules, and effectors of inflammation[5][7]. Such pathways typically integrate cell surface receptor signals (e.g., from Toll-like receptors, cytokine receptors), intracellular cascades (JAK-STAT, NF-κB, MAPK, interferon signaling), and transcription factor activation, ultimately coordinating cellular responses like immune cell recruitment, cytokine secretion, and tissue repair[5][7]. These pathways are critical for host defense, but inappropriate or chronic activation contributes to the pathogenesis of diverse diseases including autoimmune diseases, cancer, sepsis, and metabolic and neurodegenerative conditions[1][3][7]. Various gene sets and pathway databases (such as MSigDB) curate lists of canonical inflammatory pathways, and enrichment analysis of inflammatory gene expression signatures is a common approach in research to classify disease subtypes, identify prognostic markers, or explore disease mechanisms[5][1][3]. Since "inflammatory gene expression pathways" is not a single discrete molecular entity, it cannot be used directly as a therapeutic target, although individual pathway components (such as interleukin-6 receptor, Janus kinases, or NF-κB) are often targeted by specific drugs[5][7].
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