Harriet Langford, Callum Hargrove, Isla Pendleton, Rowan Tinsley, Beatrix Hammond
Macrophages are fundamental components of the immune system, orchestrating responses to pathogens, maintaining tissue integrity, and mediating repair processes. These versatile cells arise from yolk sac progenitors or monocyte precursors, differentiating into tissue-resident macrophages influenced by local microenvironments. Their functional diversity enables macrophages to adopt specific roles, ranging from pathogen clearance to the regulation of inflammation. In inflammatory diseases, such as rheumatoid arthritis, atherosclerosis, and inflammatory bowel disease, macrophage dysfunction has emerged as a critical driver of pathogenesis. Dysregulation of their polarization into pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes contributes to chronic inflammation and tissue damage. Additionally, alterations in macrophage metabolism and epigenetic profiles further exacerbate their pathological roles, disrupting the delicate balance required for immune homeostasis. Recent advancements in macrophage-targeted therapies, including strategies for functional modulation and reprogramming, are highlighted as promising approaches to mitigate inflammation-driven damage and restore immune balance. Understanding these processes offers critical insights into innovative therapeutic strategies for treating inflammatory diseases.
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