首页> 外文OA文献 >The CC chemokine ligand (CCL) 1, upregulated by the viral transactivator Tax, can be downregulated by minocycline: possible implications for long-term treatment of HTLV-1-associated myelopathy/tropical spastic paraparesis
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The CC chemokine ligand (CCL) 1, upregulated by the viral transactivator Tax, can be downregulated by minocycline: possible implications for long-term treatment of HTLV-1-associated myelopathy/tropical spastic paraparesis

机译:通过米诺环素可以下调CC趋化因子配体(CCL)1,可通过米诺环素下调:对于HTLV-1相关的肌蛋胨/热带痉挛性痉挛性痉挛的长期治疗可能的影响

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摘要

Abstract Background Chemokine (C-C motif) ligand 1 (CCL1) is produced by activated monocytes/ macrophages and T-lymphocytes, and acts as a potent attractant for Th2 cells and a subset of T-regulatory (Treg) cells. Previous reports have indicated that CCL1 is overexpressed in adult T-cell leukemia cells, mediating an autocrine anti-apoptotic loop. Because CCL1 is also known as a potent chemoattractant that plays a major role in inflammatory processes, we investigated the role of CCL1 in the pathogenesis of human T-cell leukemia virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Results The results showed that: (1) CCL1 was preferentially expressed in HAM/TSP-derived HTLV-1-infected T-cell lines, (2) CCL1 expression was induced along with Tax expression in the Tax-inducible T-cell line JPX9, (3) transient Tax expression in an HTLV-1-negative T-cell line activated the CCL1 gene promoter, (4) plasma levels of CCL1 were significantly higher in patients with HAM/TSP than in HTLV-1-seronegative patients with multiple sclerosis and HTLV-1-infected asymptomatic healthy carriers, and (5) minocycline inhibited the production of CCL1 in HTLV-1-infected T-cell lines. Conclusions The present results suggest that elevated CCL1 levels may be associated with the pathogenesis of HAM/TSP. Although further studies are required to determine the in vivo significance, minocycline may be considered as a potential candidate for the long-term treatment of HAM/TSP via its anti-inflammatory effects, which includes the inhibition of CCL1 expression.
机译:摘要背景下趋化因子(C-C图案)配体1(CCL1)由活化的单核细胞/巨噬细胞和T淋巴细胞产生,并作为TH2细胞的有效引诱剂和T-incual(Treg)细胞的子集。先前的报道表明,CCL1在成人T细胞白血病细胞中过表达,介导自分泌抗凋亡环。因为CCL1也称为在炎症过程中发挥着重要作用的有效的化学趋化剂,我们研究了CCL1在人T细胞白血病病毒1型(HTLV-1)的发病机制中的作用(HTLV-1) - 分类化肌蛋胨/热带痉挛性痉挛(火腿) / TSP)。结果结果表明:(1)CCL1优先于火腿/ TSP衍生的HTLV-1感染的T细胞系中表达,(2)CCL1表达与税收诱导的T细胞系JPX9中的税表达一起诱导(3)HTLV-1阴性T细胞中的瞬时税表达活化了CCL1基因启动子,(4)火腿/ TSP患者中CCL1的血浆水平显着高于HTLV-1-SERONEGATIVE患者硬化症和HTLV-1感染的无症状健康载体,和(5)米诺环素在HTLV-1感染的T细胞系中抑制CCL1的产生。结论本结果表明,升高的CCL1水平可能与火腿/ TSP的发病机制有关。尽管需要进一步的研究来确定体内显着性,但米诺环素可以被认为是通过其抗炎作用的长期治疗火腿/ TSP的潜在候选者,其包括抑制CCL1表达。

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