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细胞间黏附分子(ICAM)-1、ICAM-2和ICAM-3在人类免疫缺陷病毒介导的多核巨细胞形成过程中作为淋巴细胞功能相关分子1的反受体发挥作用。

Intercellular adhesion molecules (ICAM)-1 ICAM-2 and ICAM-3 function as counter-receptors for lymphocyte function-associated molecule 1 in human immunodeficiency virus-mediated syncytia formation.

作者信息

Butini L, De Fougerolles A R, Vaccarezza M, Graziosi C, Cohen D I, Montroni M, Springer T A, Pantaleo G, Fauci A S

机构信息

Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.

出版信息

Eur J Immunol. 1994 Sep;24(9):2191-5. doi: 10.1002/eji.1830240939.

Abstract

It has been previously demonstrated that lymphocyte function-associated molecule 1 (LFA-1) plays a major role in human immunodeficiency virus (HIV)-mediated syncytia formation. In the present study we investigated the involvement of intercellular adhesion molecule-1 (ICAM-1), ICAM-2 and ICAM-3 in the process. The ability of monoclonal antibodies (mAb) directed against ICAM-1, ICAM-2 and ICAM-3 to block syncytia was analyzed either in phytohemagglutinin (PHA)-activated lymphocytes infected in vitro with primary or laboratory strains of HIV or by coculturing a T cell line stably expressing HIV envelope with PHA-activated lymphocytes. Complete inhibition of syncytia formation was observed only by the simultaneous addition to the cell cultures of all (i.e. anti-ICAM-1, anti-ICAM-2 and anti-ICAM-3) mAb. These results indicate that the interaction between LFA-1 and ICAM is a critical step in HIV-mediated syncytia formation, and that ICAM-1, ICAM-2 and ICAM-3 are the receptor molecules for the LFA-1-dependent syncytia formation.

摘要

先前已经证明淋巴细胞功能相关分子1(LFA-1)在人类免疫缺陷病毒(HIV)介导的合胞体形成中起主要作用。在本研究中,我们调查了细胞间粘附分子-1(ICAM-1)、ICAM-2和ICAM-3在该过程中的参与情况。在体外感染了HIV原代或实验室毒株的植物血凝素(PHA)激活的淋巴细胞中,或者通过将稳定表达HIV包膜的T细胞系与PHA激活的淋巴细胞共培养,分析了针对ICAM-1、ICAM-2和ICAM-3的单克隆抗体(mAb)阻断合胞体的能力。仅通过向细胞培养物中同时添加所有(即抗ICAM-1、抗ICAM-2和抗ICAM-3)mAb,才观察到合胞体形成的完全抑制。这些结果表明,LFA-1与ICAM之间的相互作用是HIV介导的合胞体形成中的关键步骤,并且ICAM-1、ICAM-2和ICAM-3是LFA-1依赖性合胞体形成的受体分子。

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