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作 者:Dur E Maknoon Razia Syed Sib Tul Hassan Shah Tabish Faheem
机构地区:[1]Department of Pathogen Biology,College of Basic Medical Sciences,Jilin University,Changchun 130015,China [2]Zhejiang Province Key Laboratory of Plant Secondary Metabolism and Regulation,College of Life Sciences and Medicine,Zhejiang Sci-Tech University,Hangzhou 310018,China [3]Department of Surgery,Nishtar Medical university,Multan 66000,Pakistan.
出 处:《Life Research》2024年第4期29-41,共13页TMR生命研究
摘 要:Chronic obstructive pulmonary disease(COPD)is a multifaceted syndrome characterized by a dysregulated inflammatory cascade within the respiratory system,primarily triggered by exposure to harmful particles and gases,notably from cigarette smoke.This inflammatory response is orchestrated by innate immune cells like macrophages and epithelial cells,which recognize danger signals released from damaged cells.Prolonged inflammation prompts an adaptive immune reaction mediated by dendritic cells,culminating in the formation of lymphoid follicles and involving a complex interplay of T and B cells,as well as cytotoxic activity.Additionally,both viral and bacterial infections exacerbate COPD by further igniting inflammatory pathways,perpetuating the chronic inflammatory state.This comprehensive review encapsulates the intricate interplay between innate and adaptive immunity in COPD,with a particular focus on the role of cigarette smoke in its pathogenesis and potential therapeutic targets.
关 键 词:chronic obstructive pulmonary disease innate immunity adaptive immunity cigarette smoke inflammation oxidative stress protease-antiprotease imbalance
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