Human T-cell leukemia virus type-I Tax induces the expression of CD83 on T cells.

Human T-cell leukemia virus type-I Tax induces the expression of CD83 on T cells.
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DOI:
10.1186/s12977-015-0185-1
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发表时间:
2015-07-01
期刊:
影响因子:
3.3
通讯作者:
Nakamura M
Nakamura M
中科院分区:
医学2区
文献类型:
--
作者:
Tanaka Y;Mizuguchi M;Takahashi Y;Fujii H;Tanaka R;Fukushima T;Tomoyose T;Ansari AA;Nakamura M

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CD 83是一种在成熟树突状细胞上稳定表达的细胞表面糖蛋白,在细胞活化后可在其他造血细胞谱系上瞬时诱导。与膜形式的CD 83相反,可溶性CD 83似乎是免疫抑制性的。在对成人T细胞白血病(ATL)患者的白血病CD 4 + T细胞表型的分析中,我们发现许多原代CD 4 + T细胞在短期培养后对细胞表面CD 83呈阳性,并且这些CD 83 + CD 4 + T细胞中的大多数对人T细胞白血病病毒I型(HTLV-I)Tax(Tax 1)呈阳性。我们假设Tax 1参与了CD 83的诱导。我们发现,CD 83选择性表达在短期培养的外周血单个核细胞(PBMC)从HTLV-I+捐助者,包括ATL患者和HTLV-I携带者中分离的Tax 1表达的人CD 4 + T细胞。表达Tax 1的HTLV-I感染的T细胞系也表达细胞表面CD 83并释放可溶性CD 83。CD 83可以通过镉介导的Tax 1诱导在JPX-9细胞系中表达,并且通过用携带Tax 1基因的重组腺病毒感染导入Tax 1在Jurkat细胞或PBMC中表达。Tax 1以NF-κ B依赖性方式激活CD 83启动子。基于先前的报告显示,可溶性CD 83介导的前列腺素E2(PGE 2)的生产从人单核细胞在体外,我们测试了PGE 2是否影响HTLV-I的传播,并发现,PGE 2强烈刺激Tax 1和病毒结构分子的表达。我们的研究结果表明,HTLV-I诱导T细胞上的CD 83表达通过Tax 1介导的NF-κB活化,这可能促进HTLV-I体内感染。本文的在线版本(doi:10.1186/s12977-015-0185-1)包含补充材料,可供授权用户使用。
CD83, a cell surface glycoprotein that is stably expressed on mature dendritic cells, can be transiently induced on other hematopoietic cell lineages upon cell activation. In contrast to the membrane form of CD83, soluble CD83 appears to be immunosuppressive. In an analysis of the phenotype of leukemic CD4+ T cells from patients with adult T-cell leukemia (ATL), we found that a number of primary CD4+ T cells became positive for cell surface CD83 after short-term culture, and that most of these CD83+ CD4+ T cells were positive for human T-cell leukemia virus type-I (HTLV-I) Tax (Tax1). We hypothesized that Tax1 is involved in the induction of CD83. We found that CD83 was expressed selectively on Tax1-expressing human CD4+ T cells in short-term cultured peripheral blood mononuclear cells (PBMCs) isolated from HTLV-I+ donors, including ATL patients and HTLV-I carriers. HTLV-I-infected T cell lines expressing Tax1 also expressed cell surface CD83 and released soluble CD83. CD83 can be expressed in the JPX-9 cell line by cadmium-mediated Tax1 induction and in Jurkat cells or PBMCs by Tax1 introduction via infection with a recombinant adenovirus carrying the Tax1 gene. The CD83 promoter was activated by Tax1 in an NF-κB-dependent manner. Based on a previous report showing soluble CD83-mediated prostaglandin E2 (PGE2) production from human monocytes in vitro, we tested if PGE2 affected HTLV-I propagation, and found that PGE2 strongly stimulated expression of Tax1 and viral structural molecules. Our results suggest that HTLV-I induces CD83 expression on T cells via Tax1 -mediated NF-κB activation, which may promote HTLV-I infection in vivo. The online version of this article (doi:10.1186/s12977-015-0185-1) contains supplementary material, which is available to authorized users.
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