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H9淋巴母细胞的HIV感染会长期激活肌醇多磷酸途径。

HIV infection of H9 lymphoblastoid cells chronically activates the inositol polyphosphate pathway.

作者信息

Nye K E, Pinching A J

机构信息

Department of Immunology, St Mary's Hospital Medical School, London, UK.

出版信息

AIDS. 1990 Jan;4(1):41-5. doi: 10.1097/00002030-199001000-00006.

DOI:10.1097/00002030-199001000-00006
PMID:1969281
Abstract

Infection with HIV causes a reduction in the numbers and function of CD4+ lymphocytes and functional abnormalities of other cells. We have studied the effect of HIV infection on signal transduction in the H9 lymphoblastoid CD4+ cell line. Resting HIV-infected H9 cells show evidence of chronic activation with raised levels of InsP3 and InsP4, the active metabolites of the inositol polyphosphate pathway, and a consequently raised intracellular free calcium concentration. Stimulation of HIV-infected H9 cells with phytohemagglutinin (PHA) leads to a fall in the previously raised levels of InsP3 but a further rise in InsP4, whilst an attenuated intracellular calcium rise is seen with both PHA and anti-CD3 antibody. The observed effects of HIV infection on signal transduction provide a mechanism to explain the functional defects in CD4+ lymphocytes and, possibly, other cell types.

摘要

感染HIV会导致CD4+淋巴细胞数量减少和功能异常,以及其他细胞的功能异常。我们研究了HIV感染对H9淋巴母细胞样CD4+细胞系信号转导的影响。静止的HIV感染H9细胞显示出慢性激活的证据,肌醇多磷酸途径的活性代谢物InsP3和InsP4水平升高,因此细胞内游离钙浓度升高。用植物血凝素(PHA)刺激HIV感染的H9细胞会导致之前升高的InsP3水平下降,但InsP4进一步升高,而PHA和抗CD3抗体刺激时细胞内钙升高减弱。观察到的HIV感染对信号转导的影响为解释CD4+淋巴细胞以及可能其他细胞类型的功能缺陷提供了一种机制。

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HIV infection of H9 lymphoblastoid cells chronically activates the inositol polyphosphate pathway.H9淋巴母细胞的HIV感染会长期激活肌醇多磷酸途径。
AIDS. 1990 Jan;4(1):41-5. doi: 10.1097/00002030-199001000-00006.
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