• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

I型干扰素诱导产生抑制性16-kD CCAAT/增强子结合蛋白（C/EBP）β，从而抑制巨噬细胞中的HIV-1长末端重复序列：肺结核会改变C/EBP的表达，增强HIV-1复制。

Type I interferon induces inhibitory 16-kD CCAAT/ enhancer binding protein (C/EBP)beta, repressing the HIV-1 long terminal repeat in macrophages: pulmonary tuberculosis alters C/EBP expression, enhancing HIV-1 replication.

作者信息

Honda Y, Rogers L, Nakata K, Zhao B Y, Pine R, Nakai Y, Kurosu K, Rom W N, Weiden M

机构信息

Division of Pulmonary and Critical Care Medicine and Bellevue Chest Service, New York University Medical Center, New York 10016, USA.

出版信息

J Exp Med. 1998 Oct 5;188(7):1255-65. doi: 10.1084/jem.188.7.1255.

DOI:10.1084/jem.188.7.1255
PMID:9763605
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2212491/
Abstract

We have previously observed that HIV-1 replication is suppressed in uninflamed lung and increased during tuberculosis. In vitro THP-1 cell-derived macrophages inhibited HIV-1 replication after infection with Mycobacterium tuberculosis. Suppression of HIV-1 replication was associated with inhibition of the HIV-1 long terminal repeat (LTR) and induction of ISGF-3, a type I interferon (IFN)-specific transcription factor. Repression of the HIV-1 LTR required intact CCAAT/enhancer binding protein (C/EBP) sites. THP-1 cell-derived macrophages infected with M. tuberculosis, lipopolysaccharide, or IFN-beta induced the 16-kD inhibitory C/EBPbeta isoform and coincidentally repressed HIV-1 LTR transcription. C/EBPbeta was the predominant C/EBP family member produced in THP-1 macrophages during HIV-1 LTR repression. In vivo, alveolar macrophages from uninflamed lung strongly expressed inhibitory 16-kD C/EBPbeta, but pulmonary tuberculosis abolished inhibitory C/EBPbeta expression and induced a novel C/EBP DNA binding protein. Therefore, in vitro, proinflammatory stimulation produces an IFN response inhibiting viral replication by induction of a C/EBPbeta transcriptional repressor. THP-1 cell-derived macrophages stimulated with type I IFN are similar to alveolar macrophages in the uninflamed lung in vivo. In contrast, the cellular immune response in active pulmonary tuberculosis disrupts this innate immunity, switching C/EBP expression and allowing high level viral replication.

摘要

我们之前观察到，HIV-1在未发炎的肺部复制受到抑制，而在结核病期间则会增加。体外实验中，经结核分枝杆菌感染后的THP-1细胞来源的巨噬细胞会抑制HIV-1复制。HIV-1复制的抑制与HIV-1长末端重复序列（LTR）的抑制以及ISGF-3（一种I型干扰素（IFN）特异性转录因子）的诱导有关。HIV-1 LTR的抑制需要完整的CCAAT/增强子结合蛋白（C/EBP）位点。感染结核分枝杆菌、脂多糖或IFN-β的THP-1细胞来源的巨噬细胞会诱导16-kD抑制性C/EBPβ异构体的产生，并同时抑制HIV-1 LTR转录。C/EBPβ是HIV-1 LTR抑制期间THP-1巨噬细胞中产生的主要C/EBP家族成员。在体内，未发炎肺部的肺泡巨噬细胞强烈表达抑制性16-kD C/EBPβ，但肺结核会消除抑制性C/EBPβ的表达，并诱导一种新的C/EBP DNA结合蛋白。因此，在体外，促炎刺激通过诱导C/EBPβ转录抑制因子产生IFN反应来抑制病毒复制。经I型IFN刺激的THP-1细胞来源的巨噬细胞在体内与未发炎肺部的肺泡巨噬细胞相似。相比之下，活动性肺结核中的细胞免疫反应会破坏这种先天免疫，改变C/EBP的表达，从而允许高水平的病毒复制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/773f1715dc44/JEM980913.f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/3585f80d383d/JEM980913.f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/db780d78ee10/JEM980913.f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/3bf19130a68c/JEM980913.f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/c23f4f838e4a/JEM980913.f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/295c833010b6/JEM980913.f5ab.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/04857e98fb44/JEM980913.f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/6aa728333f63/JEM980913.f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/773f1715dc44/JEM980913.f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/3585f80d383d/JEM980913.f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/db780d78ee10/JEM980913.f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/3bf19130a68c/JEM980913.f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/c23f4f838e4a/JEM980913.f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/295c833010b6/JEM980913.f5ab.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/04857e98fb44/JEM980913.f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/6aa728333f63/JEM980913.f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b92/2212491/773f1715dc44/JEM980913.f8.jpg

相似文献

1
Type I interferon induces inhibitory 16-kD CCAAT/ enhancer binding protein (C/EBP)beta, repressing the HIV-1 long terminal repeat in macrophages: pulmonary tuberculosis alters C/EBP expression, enhancing HIV-1 replication.I型干扰素诱导产生抑制性16-kD CCAAT/增强子结合蛋白（C/EBP）β，从而抑制巨噬细胞中的HIV-1长末端重复序列：肺结核会改变C/EBP的表达，增强HIV-1复制。
J Exp Med. 1998 Oct 5;188(7):1255-65. doi: 10.1084/jem.188.7.1255.
2
Differentiation of monocytes to macrophages switches the Mycobacterium tuberculosis effect on HIV-1 replication from stimulation to inhibition: modulation of interferon response and CCAAT/enhancer binding protein beta expression.单核细胞向巨噬细胞的分化改变了结核分枝杆菌对HIV-1复制的影响，从刺激转为抑制：干扰素反应和CCAAT/增强子结合蛋白β表达的调节。
J Immunol. 2000 Aug 15;165(4):2028-39. doi: 10.4049/jimmunol.165.4.2028.
3
[Molecular pathogenesis in tuberculosis complicated with AIDS].[艾滋病合并结核病的分子发病机制]
Kekkaku. 2004 Nov;79(11):659-67.
4
[Tuberculosis in patients with acquired immune deficiency syndrome].获得性免疫缺陷综合征患者的结核病
Kekkaku. 2000 Sep;75(9):547-56.
5
Mechanisms of polymorphonuclear neutrophil-mediated induction of HIV-1 replication in macrophages during pulmonary tuberculosis.肺结核期间多形核中性粒细胞介导巨噬细胞中HIV-1复制诱导的机制
J Infect Dis. 2007 May 1;195(9):1303-10. doi: 10.1086/513438. Epub 2007 Mar 19.
6
Regulation of SIV mac 239 basal long terminal repeat activity and viral replication in macrophages: functional roles of two CCAAT/enhancer-binding protein beta sites in activation and interferon beta-mediated suppression.调控 SIVmac239 基础长末端重复序列活性和巨噬细胞中病毒复制：两个 CCAAT/增强子结合蛋白β位点在激活和干扰素β介导的抑制中的功能作用。
J Biol Chem. 2010 Jan 22;285(4):2258-73. doi: 10.1074/jbc.M109.075929. Epub 2009 Nov 20.
7
Maximal HIV-1 replication in alveolar macrophages during tuberculosis requires both lymphocyte contact and cytokines.肺结核期间肺泡巨噬细胞中HIV-1的最大复制需要淋巴细胞接触和细胞因子。
J Exp Med. 2002 Feb 18;195(4):495-505. doi: 10.1084/jem.20011614.
8
C/EBP proteins activate transcription from the human immunodeficiency virus type 1 long terminal repeat in macrophages/monocytes.C/EBP蛋白可激活巨噬细胞/单核细胞中1型人类免疫缺陷病毒长末端重复序列的转录。
J Virol. 1995 Sep;69(9):5337-44. doi: 10.1128/JVI.69.9.5337-5344.1995.
9
Mycobacterium tuberculosis enhances human immunodeficiency virus-1 replication by transcriptional activation at the long terminal repeat.结核分枝杆菌通过长末端重复序列处的转录激活增强人类免疫缺陷病毒1型的复制。
J Clin Invest. 1995 May;95(5):2324-31. doi: 10.1172/JCI117924.
10
Regulation of HIV-1 long terminal repeats by interaction of C/EBP(NF-IL6) and NF-kappaB/Rel transcription factors.通过C/EBP（NF-IL6）与NF-κB/Rel转录因子的相互作用对HIV-1长末端重复序列的调控
J Biol Chem. 1996 Sep 13;271(37):22479-86. doi: 10.1074/jbc.271.37.22479.

引用本文的文献

1
Alveolar Macrophages in Viral Respiratory Infections: Sentinels and Saboteurs of Lung Defense.病毒感染性呼吸道疾病中的肺泡巨噬细胞：肺部防御的哨兵与破坏者
Int J Mol Sci. 2025 Jan 5;26(1):407. doi: 10.3390/ijms26010407.
2
RPLP1 restricts HIV-1 transcription by disrupting C/EBPβ binding to the LTR.RPLP1 通过破坏 C/EBPβ 与 LTR 的结合来限制 HIV-1 的转录。
Nat Commun. 2024 Jun 21;15(1):5290. doi: 10.1038/s41467-024-49622-1.
3
MiR-320 inhibits PRRSV replication by targeting PRRSV ORF6 and porcine CEBPB.miR-320 通过靶向 PRRSV ORF6 和猪 CEBPB 抑制 PRRSV 复制。

本文引用的文献

1
Convergence of TNFalpha and IFNgamma signalling pathways through synergistic induction of IRF-1/ISGF-2 is mediated by a composite GAS/kappaB promoter element.通过复合GAS/κB启动子元件介导的IRF-1/ISGF-2协同诱导，实现TNFα和IFNγ信号通路的汇聚。
Nucleic Acids Res. 1997 Nov 1;25(21):4346-54. doi: 10.1093/nar/25.21.4346.
2
CCAAT/enhancer binding protein (C/EBP) sites are required for HIV-1 replication in primary macrophages but not CD4(+) T cells.CCAAT/增强子结合蛋白（C/EBP）位点是HIV-1在原代巨噬细胞而非CD4(+) T细胞中复制所必需的。
Proc Natl Acad Sci U S A. 1997 Aug 5;94(16):8714-9. doi: 10.1073/pnas.94.16.8714.
3
Vet Res. 2024 May 15;55(1):61. doi: 10.1186/s13567-024-01309-7.
4
HIV UTR, LTR, and Epigenetic Immunity.HIV UTR、LTR 和表观遗传免疫。
Viruses. 2022 May 18;14(5):1084. doi: 10.3390/v14051084.
5
IFNα and β Mediated JCPyV Suppression through C/EBPβ-LIP Isoform.IFNα 和β 通过 C/EBPβ-LIP 异构体抑制 JCPyV。
Viruses. 2021 Sep 26;13(10):1937. doi: 10.3390/v13101937.
6
The -HIV syndemic interaction: why treating infection may be crucial for HIV-1 eradication.-人类免疫缺陷病毒（HIV）共病交互作用：为何治疗感染可能对根除HIV-1至关重要。
Future Virol. 2020 Feb;15(2):101-125. doi: 10.2217/fvl-2019-0069.
7
C/EBPβ is a critical mediator of IFN-α-induced exhaustion of chronic myeloid leukemia stem cells.C/EBPβ 是 IFN-α 诱导慢性髓性白血病干细胞耗竭的关键介质。
Blood Adv. 2019 Feb 12;3(3):476-488. doi: 10.1182/bloodadvances.2018020503.
8
HIV Eradication Strategies: Implications for the Central Nervous System.HIV 根除策略：对中枢神经系统的影响。
Curr HIV/AIDS Rep. 2019 Feb;16(1):96-104. doi: 10.1007/s11904-019-00428-7.
9
Apolipoprotein E is an HIV-1-inducible inhibitor of viral production and infectivity in macrophages.载脂蛋白 E 是一种 HIV-1 诱导的巨噬细胞中病毒产生和感染性的抑制剂。
PLoS Pathog. 2018 Nov 29;14(11):e1007372. doi: 10.1371/journal.ppat.1007372. eCollection 2018 Nov.
10
A Quantitative Approach to SIV Functional Latency in Brain Macrophages.一种针对脑巨噬细胞中SIV功能潜伏期的定量方法。
J Neuroimmune Pharmacol. 2019 Mar;14(1):23-32. doi: 10.1007/s11481-018-9803-8. Epub 2018 Aug 30.
Macrophages as a source of HIV during opportunistic infections.
巨噬细胞作为机会性感染期间HIV的来源。
Science. 1997 Jun 20;276(5320):1857-61. doi: 10.1126/science.276.5320.1857.
4
Mycobacterium tuberculosis enhances human immunodeficiency virus-1 replication in the lung.结核分枝杆菌增强人类免疫缺陷病毒1型在肺部的复制。
Am J Respir Crit Care Med. 1997 Mar;155(3):996-1003. doi: 10.1164/ajrccm.155.3.9117038.
5
55- and 75-kilodalton tumor necrosis factor receptors mediate distinct actions in regard to human immunodeficiency virus type 1 replication in primary human macrophages.55千道尔顿和75千道尔顿的肿瘤坏死因子受体在原代人巨噬细胞中对1型人类免疫缺陷病毒复制介导不同作用。
J Virol. 1997 May;71(5):4150-6. doi: 10.1128/JVI.71.5.4150-4156.1997.
6
ISGF3 gamma p48, a specificity switch for interferon activated transcription factors.ISGF3γ p48，一种干扰素激活转录因子的特异性转换因子。
Cytokine Growth Factor Rev. 1996 Jun;7(1):11-7. doi: 10.1016/1359-6101(96)00005-6.
7
Immune defence in mice lacking type I and/or type II interferon receptors.缺乏I型和/或II型干扰素受体的小鼠的免疫防御
Immunol Rev. 1995 Dec;148:5-18. doi: 10.1111/j.1600-065x.1995.tb00090.x.
8
Regulation of HIV-1 long terminal repeats by interaction of C/EBP(NF-IL6) and NF-kappaB/Rel transcription factors.通过C/EBP（NF-IL6）与NF-κB/Rel转录因子的相互作用对HIV-1长末端重复序列的调控
J Biol Chem. 1996 Sep 13;271(37):22479-86. doi: 10.1074/jbc.271.37.22479.
9
Endogenous IFN-alpha beta suppresses colony-stimulating factor (CSF)-1-stimulated macrophage DNA synthesis and mediates inhibitory effects of lipopolysaccharide and TNF-alpha.内源性干扰素αβ抑制集落刺激因子（CSF）-1刺激的巨噬细胞DNA合成，并介导脂多糖和肿瘤坏死因子α的抑制作用。
J Immunol. 1996 Apr 1;156(7):2553-7.
10
C/EBP activators are required for HIV-1 replication and proviral induction in monocytic cell lines.C/EBP激活剂是单核细胞系中HIV-1复制和原病毒诱导所必需的。
Immunity. 1996 Jul;5(1):91-101. doi: 10.1016/s1074-7613(00)80313-1.