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作 者:王莎 王小芳[1] WANG Sha;WANG Xiaofang(Department of Outpatient,Baoding First Central Hospital,Baoding 071000,China)
机构地区:[1]保定市第一中心医院门诊部,河北保定071000
出 处:《医学综述》2024年第9期1058-1062,共5页Medical Recapitulate
摘 要:急性肾损伤(AKI)是全球的主要公共健康问题之一,其发病原因复杂,死亡率高。其中,免疫细胞及其分泌的炎症因子是诱导AKI发病的关键因素。2型固有淋巴细胞(ILC2)是参与2型免疫的固有淋巴细胞,在AKI中具有潜在的治疗价值,其在肾缺血再灌注损伤、顺铂或阿霉素诱导的AKI动物模型中发挥重要保护作用。白细胞介素-33是介导肾脏中ILC2扩增的关键细胞因子。然而,其作为一种警报素在自身免疫性疾病中也发挥潜在的致病作用。未来需对ILC2的生物学功能及其在AKI中发挥的保护作用机制进行更深入的研究,以期为AKI的治疗提供新靶点。Acute kidney injury(AKI)is one of the major public health problems worldwide,with complex causes of morbidity and high mortality.Immune cells and their secreted inflammatory factors are key factors inducing the onset of AKI.Group 2 innate lymphoid cells(ILC2)are innate lymphocytes involved in type 2 immunity and have potential therapeutic value in AKI,which play an important protective role in renal ischemia-reperfusion injury,cisplatin or adriamycin-induced AKI animal models.Interleukin-33 is a key cytokine mediating ILC2 expansion in the kidney.However,as an alarmin,it also plays a potential pathogenic role in autoimmune diseases.In the future,more in-depth research is needed on the biological functions of ILC2 and its protective mechanisms in AKI,in order to provide new targets for the treatment of AKI.
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