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首页> 外文期刊>Scandinavian journal of immunology. >Infection of Human Mononuclear Phagocytes and Macrophage-Like THP1 Cells with Leishmania donovani Results in Modulation of Expression of a Subset of Chemokines and a Chemokine Receptor.
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Infection of Human Mononuclear Phagocytes and Macrophage-Like THP1 Cells with Leishmania donovani Results in Modulation of Expression of a Subset of Chemokines and a Chemokine Receptor.

机译:人多核利什曼原虫感染人单核吞噬细胞和巨噬细胞样THP1细胞导致趋化因子亚基和趋化因子受体表达的调节。

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摘要

The expression of chemokines and chemokine receptors was studied in Leishmania donovani (LD)-infected human mononuclear phagocytes and the human monocytic cell line THP1. Our studies showed that LD infection caused the upregulation of three beta chemokines (macrophage inflammatory protein-1 alpha (MIP-1alpha), MIP-1beta and RANTES (regulated on activation normal T cell expressed and secreted)), one alpha chemokine (interleukin-8 (IL-8)) and the CC chemokine receptor 5 (CCR5) but not CCR1, as evident from reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. The CCR5 upregulation in human mononuclear phagocytes and THP1 cells was also evident by confocal microscopy. The possible association of such upregulation in relation to Leishmania and human immunodeficiency virus (HIV) coinfection was discussed.
机译:在感染了利什曼原虫(LD)的人单核吞噬细胞和人单核细胞系THP1中研究了趋化因子和趋化因子受体的表达。我们的研究表明,LD感染导致三种β趋化因子(巨噬细胞炎性蛋白1α(MIP-1alpha),MIP-1beta和RANTES(受激活的正常T细胞表达和分泌的调节)),一种α趋化因子(白介素-从逆转录酶-聚合酶链反应(RT-PCR)分析可以明显看出,图8(IL-8))和CC趋化因子受体5(CCR5)却没有CCR1。通过共聚焦显微镜也可明显观察到人单核吞噬细胞和THP1细胞中CCR5的上调。讨论了与利什曼原虫症和人类免疫缺陷病毒(HIV)合并感染有关的这种上调的可能关联。

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