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作 者:李晓晖 马秀兰[2] 马建萍[2] LI Xiao-hui;MA Xiu-lan;MA Jian-ping(The Fourth Clinical Medical College of Xinjiang Medical University,Urumqi,Xinjiang 830000,China;Hospital of Traditional Chinese Medicine Affiliated to Xinjiang Medical University,Urumqi,Xinjiang 830000,China)
机构地区:[1]新疆医科大学第四临床医学院,新疆乌鲁木齐830000 [2]新疆医科大学附属中医医院,新疆乌鲁木齐830000
出 处:《中国热带医学》2021年第5期485-489,共5页China Tropical Medicine
基 金:国家自然科学基金(No.81960798)。
摘 要:抗病毒治疗降低了艾滋病机会性感染的死亡率,然而无法改善病毒潜伏后诱导的免疫耗竭。随着负性调节分子在癌症及慢性感染性疾病方面的研究,学者们发现这些分子在艾滋病免疫调节方面同样起着重要作用。其中程序性细胞死亡受体1(programmed cell death receptor-1, PD-1)与T细胞免疫球蛋白和黏蛋白结构域3(T cell immuno-globulin and mucin domain-3, Tim-3)受到广泛的关注,在慢性人类免疫缺陷病毒(human immunodeficiency virus, HIV)感染过程中,PD-1和Tim-3及其配体高表达的抗原持续刺激是导致免疫耗竭的主要原因之一,PD-1和Tim-3被认为是免疫耗竭的标记物,可以推进获得性免疫缺陷综合征(acquired immune deficiency syndrome, AIDS)疾病进展,利用免疫检查点分子阻滞剂阻断其信号通路可以缩短潜伏期,打破病毒储存库。本综述概览了PD-1和Tim-3及其配体关于艾滋病方面的最新研究、针对PD-1/Tim-3对AIDS疾病进展的影响以及PD-1/PD-L1阻断治疗的疗效与安全性。Antiviral therapy can reduce the mortality of opportunistic HIV,but cannot improve the immune exhaustion induced by latent virus.With the research of negative regulatory molecules in cancer and chronic infectious diseases,scholars found that these molecules also play an important role in the immune regulation of acquired immune deficiency syndrome(AIDS).Among them,programmed cell death receptor-1 (PD-1) and T-cell immunoglobulin and mucin domain-3 (Tim-3) are concerned.In the process of chronic human immunodeficiency virus (HIV) infection,continuous stimulation of PD-1,Tim-3and their ligands is one of the main causes of immune exhaustion.PD-1 and Tim-3 are considered as markers of immune exhaustion and can promote AIDS progression,the use of immune checkpoint molecular blockers to block its signal pathway can shorten the incubation period,and break off the virus repository.This article summarized the latest researches on AIDS related to PD-1,Tim-3 and their ligands in the past three years.The impacts of PD-1/Tim-3 on the progression of AIDS and the efficacy and safety of PD-1/PD-L1 blocking therapy,were reviewed.
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