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HIV导致单核细胞系中CD44表达缺失。

HIV-induced loss of CD44 expression in monocytic cell lines.

作者信息

Guo M M, Hildreth J E

机构信息

Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205.

出版信息

J Immunol. 1993 Aug 15;151(4):2225-36.

PMID:8345206
Abstract

We have found that HIV-1 infection of monocytic cell lines results in a new adhesion phenotype. Whereas uninfected cells grow as single cell suspensions, HIV-infected cells grow as large aggregates. When the expression of adhesion molecules was investigated, CD44 was almost completely depleted from the surface of HIV-infected cells. Immunoprecipitation with mAb confirmed the loss of CD44 from the surface of infected cells. In addition, loss of surface CD44 was not due to formation of internal complexes or release into the culture supernatant. Soluble CD44 was not detected in culture supernatant from HIV-infected cells. Northern blot analysis showed an altered RNA pattern in HIV-infected cells. The high molecular mass CD44 RNA (7.0 kb) was lost from infected cells, and the low molecular mass CD44 RNA (1.2 kb) remained. We have previously shown that anti-CD44 mAb induces homotypic adhesion in CD44+ cell lines. In this report, we show that homotypic adhesion of the HIV-infected cells occurs through a different mechanism than anti-CD44 mAb-induced aggregation. The homotypic adhesion in infected cells was CD18-mediated, but anti-CD44 mAb-induced homotypic adhesion in uninfected cells was CD18-independent. The change in adhesion phenotype and the loss of CD44 from the surface of HIV-1-infected monocytic cells are discussed in terms of their potential implications in cell-to-cell transmission of HIV.

摘要

我们发现,HIV-1感染单核细胞系会导致一种新的黏附表型。未感染的细胞以单细胞悬液形式生长,而HIV感染的细胞则聚集成大的细胞团生长。当研究黏附分子的表达时,CD44几乎从HIV感染细胞的表面完全缺失。用单克隆抗体进行免疫沉淀证实了感染细胞表面CD44的缺失。此外,表面CD44的缺失并非由于形成内部复合物或释放到培养上清液中。在HIV感染细胞的培养上清液中未检测到可溶性CD44。Northern印迹分析显示HIV感染细胞中的RNA模式发生了改变。感染细胞中高分子量的CD44 RNA(7.0 kb)消失,而低分子量的CD44 RNA(1.2 kb)仍然存在。我们之前已经表明,抗CD44单克隆抗体可诱导CD44+细胞系中的同型黏附。在本报告中,我们表明HIV感染细胞的同型黏附通过与抗CD44单克隆抗体诱导的聚集不同的机制发生。感染细胞中的同型黏附是由CD18介导的,但未感染细胞中抗CD44单克隆抗体诱导的同型黏附不依赖于CD18。我们将根据HIV-1感染的单核细胞表面黏附表型的变化和CD44的缺失对HIV细胞间传播的潜在影响进行讨论。

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