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一种白细胞脂质上调淋巴细胞功能相关抗原-1的亲和力。

A leukocyte lipid up-regulates the avidity of lymphocyte function-associated antigen-1.

作者信息

Lee D H, MacIntyre J P, Wang E, Hudson D J, Ishaque A, Conant J A, Pope B L, Lau C Y

机构信息

R.W. Johnson Pharmaceutical Research Institute, Don Mills, Ontario, Canada.

出版信息

Biochem Biophys Res Commun. 1994 Feb 28;199(1):319-26. doi: 10.1006/bbrc.1994.1231.

Abstract

An acidic lipid termed leukocyte adhesion lipid (LAL) was isolated from PMA stimulated lymphoid and myeloid cell lines HL60, Jurkat, K562 and U937 but not from unstimulated cells or PMA treated Cos7 cells. LAL treated peripheral blood leukocytes (PBL) adhered strongly to IL-1 beta activated human umbilical vein endothelial cells (HUVEC), and the interaction could be inhibited by antibodies to intercellular adhesion molecule (ICAM-1) or lymphocyte function-associated antigen-1 (LFA-1). Leukocytes treated with LAL maintained the high avidity state of LFA-1 for at least 1 hr whereas the avidity of LFA-1 in PMA treated cells declined after 30 min. LAL was stable to heat (100 degrees C, 10 min), alkaline phosphatase and proteinase K treatments. Chemical analysis suggested that LAL contained unsaturated lipids. Our findings provide evidence for the involvement of lipids in LFA-1 activation.

摘要

一种名为白细胞黏附脂质(LAL)的酸性脂质是从经佛波酯(PMA)刺激的淋巴样和髓样细胞系HL60、Jurkat、K562和U937中分离得到的,但未从不经刺激的细胞或经PMA处理的Cos7细胞中分离得到。LAL处理的外周血白细胞(PBL)能强烈黏附于白细胞介素-1β(IL-1β)激活的人脐静脉内皮细胞(HUVEC),且这种相互作用可被细胞间黏附分子(ICAM-1)或淋巴细胞功能相关抗原-1(LFA-1)的抗体所抑制。用LAL处理的白细胞使LFA-1维持高亲和力状态至少1小时,而经PMA处理的细胞中LFA-1的亲和力在30分钟后下降。LAL对热(100℃,10分钟)、碱性磷酸酶和蛋白酶K处理均稳定。化学分析表明LAL含有不饱和脂质。我们的研究结果为脂质参与LFA-1激活提供了证据。

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