炎症
免疫学
免疫系统
趋化因子
模式识别受体
获得性免疫系统
关节炎
医学
急性呼吸窘迫综合征
免疫
生物
先天免疫系统
肺
内科学
标识
DOI:10.1016/j.intimp.2019.05.002
摘要
Inflammation occurs as a result of acute trauma, invasion of the host by different pathogens, pathogen-associated molecular patterns (PAMPs) or chronic cellular stress generating damage-associated molecular patterns (DAMPs). Thus inflammation may occur under both sterile inflammatory conditions including certain cancers, autoimmune or autoinflammatory diseases (Rheumatic arthritis (RA)) and infectious diseases including sepsis, pneumonia-associated acute lung inflammation (ALI) or acute respiratory distress syndrome (ARDS). The pathogenesis of inflammation involves dysregulation of an otherwise protective immune response comprising of various innate and adaptive immune cells and humoral (cytokines and chemokines) mediators secreted by these immune cells upon the activation of signaling mechanisms regulated by the activation of different pattern recognition receptors (PRRs). However, the pro-inflammatory and anti-inflammatory action of these immune cells is determined by the metabolic stage of the immune cells. The metabolic process of immune cells is called immunometabolism and its shift determined by inflammatory stimuli is called immunometabolic reprogramming. The article focuses on the involvement of various immune cells generating the inflammation, their interaction, immunometabolic reprogramming, and the therapeutic targeting of the immunometabolism to manage inflammation.
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