摘要
炎症和纤维化是两种相互关联的疾病病理学,具有几个重叠的成分。三种特定的细胞类型,即巨噬细胞、T 辅助细胞和肌成纤维细胞,在调节这两个过程中起重要作用。组织损伤后,通常需要炎症刺激来启动组织修复,其中从浸润和驻留的免疫和炎症细胞释放的细胞因子刺激产生细胞外基质的肌成纤维细胞的增殖和活化。然而,持续的组织损伤会导致不适当的促纤维化反应。此外,活化的肌成纤维细胞可以承担传统抗原呈递细胞的作用,分泌促炎细胞因子,并将炎症细胞募集到纤维化病灶,从而在恶性循环中放大纤维化反应。此外,炎症细胞已被证明在纤维化疾病过程的启动、放大和消退中发挥着相互矛盾的作用。炎症小体分子平台在促进纤维化中的核心作用才刚刚开始被充分认识。在这篇综述中,我们讨论了可导致纤维化的免疫机制,在对损伤的免疫反应背景下与纤维化过程有关的炎症小体,并讨论了针对炎症小体诱导的胶原沉积的当前和新兴疗法治疗器官纤维化。
关键词: 免疫机制、炎性体、NLRP3炎性体、肌成纤维细胞分化、胶原沉积、纤维化
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