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CD4+ CD25+ regulatory T cells impair HIV-1-specific CD4 T cell responses by upregulating interleukin-10 production in monocytes.CD4+ CD25+ 调节性 T 细胞通过上调单核细胞中白细胞介素-10 的产生来损害 HIV-1 特异性 CD4 T 细胞反应。
J Virol. 2012 Jun;86(12):6586-94. doi: 10.1128/JVI.06251-11. Epub 2012 Apr 11.
2
The influence of HIV on CD127 expression and its potential implications for IL-7 therapy.HIV 对 CD127 表达的影响及其对 IL-7 治疗的潜在影响。
Semin Immunol. 2012 Jun;24(3):231-40. doi: 10.1016/j.smim.2012.02.006. Epub 2012 Mar 14.
3
HIV-1 proteins preferentially activate anti-inflammatory M2-type macrophages.HIV-1 蛋白优先激活抗炎型 M2 型巨噬细胞。
J Immunol. 2012 Apr 15;188(8):3620-7. doi: 10.4049/jimmunol.1101593. Epub 2012 Mar 9.
4
HIV-induced T-cell activation/exhaustion in rectal mucosa is controlled only partially by antiretroviral treatment.HIV 引起的直肠黏膜 T 细胞激活/耗竭仅部分受抗逆转录病毒治疗的控制。
PLoS One. 2012;7(1):e30307. doi: 10.1371/journal.pone.0030307. Epub 2012 Jan 19.
5
Safety and immunogenicity of an HIV-1 gag DNA vaccine with or without IL-12 and/or IL-15 plasmid cytokine adjuvant in healthy, HIV-1 uninfected adults.HIV-1 gag DNA 疫苗联合白细胞介素-12 和/或白细胞介素-15 质粒细胞因子佐剂与单独使用 HIV-1 gag DNA 疫苗在健康、未感染 HIV-1 的成年人中的安全性和免疫原性。
PLoS One. 2012;7(1):e29231. doi: 10.1371/journal.pone.0029231. Epub 2012 Jan 5.
6
Role of PD-1 in HIV pathogenesis and as target for therapy.PD-1 在 HIV 发病机制中的作用及其作为治疗靶点。
Curr HIV/AIDS Rep. 2012 Mar;9(1):81-90. doi: 10.1007/s11904-011-0106-4.
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A push-pull vaccine strategy using Toll-like receptor ligands, IL-15, and blockade of negative regulation to improve the quality and quantity of T cell immune responses.采用 Toll 样受体配体、IL-15 和阻断负调控的推拉疫苗策略来改善 T 细胞免疫应答的质量和数量。
Vaccine. 2012 Jun 19;30(29):4323-7. doi: 10.1016/j.vaccine.2011.11.034. Epub 2011 Nov 21.
8
Interleukin-21 administration to rhesus macaques chronically infected with simian immunodeficiency virus increases cytotoxic effector molecules in T cells and NK cells and enhances B cell function without increasing immune activation or viral replication.白细胞介素-21 给药恒河猴慢性感染猴免疫缺陷病毒增加细胞毒性效应分子在 T 细胞和 NK 细胞和增强 B 细胞功能而不增加免疫激活或病毒复制。
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9
Phenotype, effector function, and tissue localization of PD-1-expressing human follicular helper T cell subsets.表达 PD-1 的人滤泡辅助 T 细胞亚群的表型、效应功能和组织定位。
BMC Immunol. 2011 Sep 13;12:53. doi: 10.1186/1471-2172-12-53.
10
Increased frequency of regulatory T cells accompanies increased immune activation in rectal mucosae of HIV-positive noncontrollers.HIV 阳性非感染者的直肠黏膜中调节性 T 细胞频率增加伴随免疫激活增强。
J Virol. 2011 Nov;85(21):11422-34. doi: 10.1128/JVI.05608-11. Epub 2011 Aug 31.

细胞因子产生和失调在 HIV 发病机制中的作用:对治疗方法和疫苗开发的启示。

Cytokine production and dysregulation in HIV pathogenesis: lessons for development of therapeutics and vaccines.

机构信息

Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

出版信息

Cytokine Growth Factor Rev. 2012 Aug-Oct;23(4-5):181-91. doi: 10.1016/j.cytogfr.2012.05.005. Epub 2012 Jun 27.

DOI:10.1016/j.cytogfr.2012.05.005
PMID:22743036
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3582023/
Abstract

Numerous studies have characterized the cytokine modulation observed in human immunodeficiency virus (HIV) infected individuals, from initial infection through chronic disease. Progressive and non-progressive HIV infection models show the cytokine milieu differs in terms of production and responsiveness in these two groups, suggesting an understanding of the role cytokines play during infection is necessary for directing the immune response toward viral control. This review will cover cytokine induction and dysfunction during HIV pathogenesis, with a focus on the interplay between cytokines and transcription factors, T cell activation, and exhaustion. We highlight cytokines that have either vaccine adjuvant or therapeutic potential and discuss the need to identify key factors required for prevention of progression, clearance of infection, or protection from acquisition.

摘要

许多研究已经描述了从初始感染到慢性疾病期间在人类免疫缺陷病毒 (HIV) 感染者中观察到的细胞因子调节。进展性和非进展性 HIV 感染模型表明,这两组在细胞因子环境方面的产生和反应性存在差异,这表明了解细胞因子在感染过程中所起的作用对于指导免疫反应以实现病毒控制是必要的。本综述将涵盖 HIV 发病机制过程中的细胞因子诱导和功能障碍,重点讨论细胞因子与转录因子、T 细胞激活和耗竭之间的相互作用。我们强调了具有疫苗佐剂或治疗潜力的细胞因子,并讨论了需要确定预防进展、清除感染或防止获得所需的关键因素。