艾滋病毒感染期间 MDSC 的扩增:调节器、抗逆转录病毒疗法和免疫重建

IF 5 3区 医学 Q1 GENETICS & HEREDITY
Mahmoud Mohammad Yaseen, Nizar Mohammad Abuharfeil, Homa Darmani
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引用次数: 0

摘要

在包括人类免疫缺陷病毒(HIV)感染在内的不同病理情况下,髓源性抑制细胞(MDSCs)会发生扩增,这可能会恶化疾病状况并加速疾病进展。在 HIV 感染中,MDSCs 会抑制抗 HIV 免疫反应,阻碍免疫重建。了解 HIV 感染期间 MDSC 扩增的因素和机制对于理解 HIV 感染的病理生理学至关重要。这可能为开发新的治疗靶点或策略铺平道路。在这项工作中,我们探讨了(i)调节 MDSC 扩增的机制;(ii)抗逆转录病毒疗法(ART)对 HIV 感染期间 MDSCs 频率的影响;(iii)成功抗逆转录病毒疗法期间 MDSCs 对免疫重建的影响;以及(iv)MDSCs 作为治疗靶点的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

MDSC expansion during HIV infection: regulators, ART and immune reconstitution

MDSC expansion during HIV infection: regulators, ART and immune reconstitution

MDSC expansion during HIV infection: regulators, ART and immune reconstitution
Myeloid-derived suppressor cells (MDSCs) become expanded in different pathological conditions including human immunodeficiency virus (HIV) infection and this may worsen the disease status and accelerate disease progression. In HIV infection, MDSCs suppress anti-HIV immune responses and hamper immune reconstitution. Understanding the factors and mechanisms of MDSC expansion during HIV infection is central to understanding the pathophysiology of HIV infection. This may pave the way to developing new therapeutic targets or strategies. In this work we addressed (i) the mechanisms that regulate MDSC expansion, (ii) the impact of antiretroviral therapy (ART) on the frequency of MDSCs during HIV infection; (iii) the impact of MDSCs on immune reconstitution during successful ART; and (iv) the potential of MDSCs as a therapeutic target.
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来源期刊
Genes and immunity
Genes and immunity 医学-免疫学
CiteScore
8.90
自引率
4.00%
发文量
28
审稿时长
6-12 weeks
期刊介绍: Genes & Immunity emphasizes studies investigating how genetic, genomic and functional variations affect immune cells and the immune system, and associated processes in the regulation of health and disease. It further highlights articles on the transcriptional and posttranslational control of gene products involved in signaling pathways regulating immune cells, and protective and destructive immune responses.
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