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Transcriptomic analysis of KSHV-infected primary oral fibroblasts: The role of interferon-induced genes in the latency of oncogenic virus.卡波西肉瘤相关疱疹病毒感染的原代口腔成纤维细胞的转录组分析:干扰素诱导基因在致癌病毒潜伏中的作用
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HIV-associated cancers and lymphoproliferative disorders caused by Kaposi sarcoma herpesvirus and Epstein-Barr virus.人类免疫缺陷病毒相关癌症和卡波西肉瘤疱疹病毒与 Epstein-Barr 病毒引起的淋巴组织增生性疾病。
Clin Microbiol Rev. 2024 Sep 12;37(3):e0002223. doi: 10.1128/cmr.00022-23. Epub 2024 Jun 20.
2
Transcriptional landscape of Kaposi sarcoma tumors identifies unique immunologic signatures and key determinants of angiogenesis.卡波西肉瘤肿瘤的转录组图谱确定了独特的免疫特征和血管生成的关键决定因素。
J Transl Med. 2023 Sep 22;21(1):653. doi: 10.1186/s12967-023-04517-5.
3
KSHV infection skews macrophage polarisation towards M2-like/TAM and activates Ire1 α-XBP1 axis up-regulating pro-tumorigenic cytokine release and PD-L1 expression.卡波西肉瘤相关疱疹病毒(KSHV)感染使巨噬细胞向 M2 样/TAM 极化,并激活 Ire1α-XBP1 轴,上调促肿瘤细胞因子的释放和 PD-L1 的表达。
Br J Cancer. 2020 Jul;123(2):298-306. doi: 10.1038/s41416-020-0872-0. Epub 2020 May 18.
4
Lack of CD8 T-cell co-localization with Kaposi's sarcoma-associated herpesvirus infected cells in Kaposi's sarcoma tumors.在卡波西肉瘤肿瘤中,CD8 T细胞与卡波西肉瘤相关疱疹病毒感染细胞缺乏共定位。
Oncotarget. 2020 Apr 28;11(17):1556-1572. doi: 10.18632/oncotarget.27569.
5
Determining cell type abundance and expression from bulk tissues with digital cytometry.利用数字细胞术从组织样本中测定细胞类型丰度和表达。
Nat Biotechnol. 2019 Jul;37(7):773-782. doi: 10.1038/s41587-019-0114-2. Epub 2019 May 6.
6
Kaposi's sarcoma-associated herpesvirus infection promotes differentiation and polarization of monocytes into tumor-associated macrophages.卡波氏肉瘤相关疱疹病毒感染促进单核细胞向肿瘤相关巨噬细胞的分化和极化。
Cell Cycle. 2017;16(17):1611-1621. doi: 10.1080/15384101.2017.1356509. Epub 2017 Jul 27.
7
Macrophage Polarization in Virus-Host Interactions.病毒-宿主相互作用中的巨噬细胞极化
J Clin Cell Immunol. 2015 Apr;6(2). doi: 10.4172/2155-9899.1000311.
8
The M1 and M2 paradigm of macrophage activation: time for reassessment.巨噬细胞活化的M1和M2范式:是时候重新评估了。
F1000Prime Rep. 2014 Mar 3;6:13. doi: 10.12703/P6-13. eCollection 2014.
9
Kaposi's sarcoma-associated herpesvirus infection of endothelial cells inhibits neutrophil recruitment through an interleukin-6-dependent mechanism: a new paradigm for viral immune evasion.卡波西肉瘤相关疱疹病毒感染内皮细胞通过白细胞介素 6 依赖性机制抑制中性粒细胞募集:病毒免疫逃避的新范例。
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Highly selective escape from KSHV-mediated host mRNA shutoff and its implications for viral pathogenesis.从卡波西肉瘤相关疱疹病毒介导的宿主mRNA关闭中高度选择性逃逸及其对病毒发病机制的影响。
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对卡波西肉瘤病变中肿瘤浸润免疫细胞的分析发现巨噬细胞群体发生了变化。

Analysis of tumor infiltrating immune cells in Kaposi sarcoma lesions discovers shifts in macrophage populations.

作者信息

Tagawa Takanobu, Mahesh Guruswamy, Ziegelbauer Joseph M

机构信息

HIV and AIDS Malignancy Branch, National Cancer Institute, Bethesda, MD, USA.

出版信息

Glob Health Med. 2024 Oct 31;6(5):310-315. doi: 10.35772/ghm.2024.01066.

DOI:10.35772/ghm.2024.01066
PMID:39483448
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11514630/
Abstract

Limited information exists about the types of immune cells present in Kaposi sarcoma (KS) lesions, especially in KS in the gastrointestinal tract. Using previously reported RNA-sequencing results from Kaposi sarcoma lesions in skin and gastrointestinal tract with normal matched tissues from the same patients at the same time, we investigated changes in lymphocytes in these tissues. We employed a computational method that determines changes in cell type distributions using KS lesion transcriptome data compared to a reference set of RNA expression patterns of purified immune cells. Since secreted cytokines and chemokines from KSHV-infected cells may influence the microenvironment of Kaposi sarcoma lesions, we performed cytokine profiling of conditioned media from KSHV-infected primary human dermal lymphatic endothelial cells. We also measured how this conditioned media altered the differentiation of macrophages in cell culture assays. These results suggested that factors in conditioned media from KSHV-infected endothelial cells promoted differentiation of a promonocytic cell line to proinflammatory macrophages.

摘要

关于卡波西肉瘤(KS)病变中存在的免疫细胞类型,尤其是胃肠道KS中的免疫细胞类型,目前所知信息有限。利用先前报道的来自皮肤和胃肠道卡波西肉瘤病变以及同一患者同一时间匹配的正常组织的RNA测序结果,我们研究了这些组织中淋巴细胞的变化。我们采用了一种计算方法,该方法通过将KS病变转录组数据与纯化免疫细胞的RNA表达模式参考集进行比较,来确定细胞类型分布的变化。由于来自感染KSHV的细胞分泌的细胞因子和趋化因子可能会影响卡波西肉瘤病变的微环境,我们对来自感染KSHV的原代人真皮淋巴管内皮细胞的条件培养基进行了细胞因子分析。我们还在细胞培养试验中测量了这种条件培养基如何改变巨噬细胞的分化。这些结果表明,来自感染KSHV的内皮细胞的条件培养基中的因子促进了原单核细胞系向促炎巨噬细胞的分化。