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首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Human T-cell leukemia virus type I infection of monocytes and microglial cells in primary human cultures.
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Human T-cell leukemia virus type I infection of monocytes and microglial cells in primary human cultures.

机译：人类T细胞白血病病毒I型感染原代人类培养物中的单核细胞和小胶质细胞。

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摘要

The pathogenesis of progressive spastic paraparesis [HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP)], a serious consequence of human T-cell leukemia virus type I (HTLV-I) infection, is unclear. T and B lymphocytes can be naturally infected by HTLV-I, but the susceptibility to HTLV-I infection of other cell types that could contribute to the pathogenesis of HAM/TSP has not been determined. We found that a human monocyte cell line (THP-1), primary human peripheral blood monocytes, and isolated microglial cells but not astrocytes or oligodendroglial cells derived from adult human brain were infected by HTLV-I in vitro. Infection with HTLV-I enhanced the secretion of interleukin 6 in human microglial cell-enriched cultures but did not stimulate the release of interleukin 1 from monocytes or microglial cells. Tumor necrosis factor alpha production was stimulated by HTLV-I infection of monocytes and microglial cells and could be enhanced by suboptimal amounts of lipopolysaccharide. Since both tumor necrosis factor alpha and interleukin 6 have been implicated in inflammatory demyelination and gliosis, our findings suggest that human microglial cells and monocytes infected with and activated by HTLV-I could play a role in the pathogenesis of HAM/TSP.
机译：尚不清楚进展性痉挛性轻瘫的发病机理[HTLV-1相关性脊髓病/热带痉挛性轻瘫（HAM / TSP）]，这是人I型T细胞白血病病毒（HTLV-1）感染的严重后果。 T和B淋巴细胞可以被HTLV-1自然感染，但是尚未确定可能导致HAM / TSP发病的其他类型细胞对HTLV-1感染的敏感性。我们发现，HTLV-1在体外感染了人单核细胞系（THP-1），原代人外周血单核细胞和分离的小胶质细胞，但未感染源自成年人脑的星形胶质细胞或少突胶质细胞。 HTLV-1感染可增强人小胶质细胞丰富培养物中白细胞介素6的分泌，但不会刺激白细胞或小胶质细胞释放白细胞介素1。 HTLV-I感染单核细胞和小胶质细胞会刺激肿瘤坏死因子α的产生，而次最佳量的脂多糖可能会增强肿瘤坏死因子α的产生。由于肿瘤坏死因子α和白介素6均与炎症性脱髓鞘和神经胶质增生有关，因此我们的发现表明，感染HTLV-1的人小神经胶质细胞和单核细胞可能在HAM / TSP的发病机理中起作用。

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