IFN-gamma regulates murine interferon-inducible T cell alpha chemokine (I-TAC) expression in dendritic cell lines and during experimental autoimmune encephalomyelitis (EAE).

IFN-gamma regulates murine interferon-inducible T cell alpha chemokine (I-TAC) expression in dendritic cell lines and during experimental autoimmune encephalomyelitis (EAE).
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IFN-gamma 调节树突状细胞系中和实验性自身免疫性脑脊髓炎 (EAE) 期间的鼠干扰素诱导 T 细胞 α 趋化因子 (I-TAC) 表达。

DOI:
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发表时间:
2002
影响因子:
3.7
通讯作者:
Scott Thomson
Scott Thomson
中科院分区:
医学4区
文献类型:
--
作者:
N. H. R. Hamilton;J. Banyer;A. Hapel;S. Mahalingam;Alistair J. Ramsay;I. Ramshaw;Scott Thomson

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鼠干扰素诱导的T细胞α趋化因子(I-TAC)是一种有效的非ELR Cys-X-Cys(CXC)趋化因子,其主要吸引活化的T淋巴细胞并结合受体CXCR 3。使用半定量逆转录-聚合酶链反应(RT-PCR),我们分析了小鼠I-TAC的表达在两个不同的祖树突状细胞(DC)系,MTHC-D2和JAWS II暴露于各种细胞因子,和Con A激活的脾细胞从一组基因敲除小鼠。对祖细胞DC系和Con A培养物的分析表明,鼠I-TAC主要通过干扰素调节因子(IRF)-1受干扰素(IFN)-γ调节。已经提出I-TAC可能在自身免疫性疾病如多发性硬化症(MS)中起作用。由于I-TAC似乎是由抗原呈递细胞(APC)分泌并吸引活化的T细胞,因此我们检测了患有髓鞘少突胶质细胞糖蛋白(MOG)35-55肽诱导的实验性自身免疫性脑脊髓炎(EAE)的野生型和IFN-γ受体敲除(IFN-γ R-/-)小鼠的中枢神经系统(CNS)中小鼠I-TAC mRNA的水平。在第14天,当小鼠开始恢复时,在野生型小鼠中检测到I-TAC表达峰值,而在IFN-gammaR-/-小鼠的中枢神经系统中检测到非常低水平的I-TAC,这些小鼠发生严重的EAE并死亡。小鼠I-TAC的表达特征表明,它是免疫细胞通讯的重要介质,可以增强疫苗和自身免疫治疗。
Murine interferon-inducible T cell alpha chemokine (I-TAC) is a potent non-ELR Cys-X-Cys (CXC) chemokine that predominantly attracts activated T lymphocytes and binds to the receptor CXCR3. Using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) we analysed murine I-TAC expression in two different progenitor dendritic cell (DC) lines, MTHC-D2 and JAWS II which were exposed to various cytokines, and Con A-activated splenocytes from a panel of knockout mice. Analysis of the progenitor DC lines and Con A cultures demonstrated that murine I-TAC is primarily regulated by interferon (IFN)-gamma via interferon regulatory factor (IRF)-1. It has been proposed that I-TAC may have a role in autoimmune diseases such as multiple sclerosis (MS). Because I-TAC appears to be secreted from antigen-presenting cells (APCs) and attracts activated T cells, we examined the level of murine I-TAC mRNA in the central nervous system (CNS) of wild-type and IFN-gamma-receptor knockout (IFN-gammaR-/-) mice with myelin oligodendrocyte glycoprotein (MOG)35-55 peptide-induced experimental autoimmune encephalomyelitis (EAE). Peak I-TAC expression was detected in wild-type mice on day 14 when the mice begin to recover, whereas very low levels of I-TAC were detected in the CNS of IFN-gammaR-/- mice which develop severe EAE and die. The expression characteristics of murine I-TAC suggest an important mediator of immune cell communication that could augment vaccines and autoimmune therapies.
DOI: 10.1172/jci6993
发表时间: 1999-10-01
影响因子: 15.9
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期刊: SCIENCE
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DOI: 10.4049/jimmunol.162.6.3549
发表时间: 1999-03
影响因子: 4.4
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实验性变态反应性脑脊髓炎大鼠中枢神经系统CSF-1、c-fms和MCP-1的表达
DOI: --
发表时间: 1993
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
Hulkower,K;Brosnan,CF;Aquino,DA;Cammer,W;Kulshrestha,S;Guida,MP;Rapoport,DA;Berman,JW
通讯作者: Berman,JW