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白细胞介素4和肿瘤坏死因子α在内皮细胞中诱导不同的黏附途径,以实现外周血淋巴细胞的结合。

Interleukin 4 and tumour necrosis factor alpha induce different adhesion pathways in endothelial cells for the binding of peripheral blood lymphocytes.

作者信息

Galéa P, Lebranchu Y, Thibault G, Bardos P

机构信息

Laboratoire d'Immunologie, CHU Bretonneau, Université de Tours, France.

出版信息

Scand J Immunol. 1992 Oct;36(4):575-85. doi: 10.1111/j.1365-3083.1992.tb03226.x.

Abstract

We demonstrated that tumour necrosis factor alpha (TNF-alpha) and interleukin 4 (IL-4) increased endothelial cell (EC) adhesiveness for peripheral blood lymphocytes (PBL) by promoting transcription and protein synthesis. The different kinetics observed with TNF-alpha and IL-4 suggest the involvement of different adhesion molecules. Blocking adhesion assays and immunofluorescence analysis showed that PBL adhesion to endothelial cells involves different pair adhesion molecules. Whereas IL-4 promoted an LFA-1-dependent/ICAM-1-independent adhesion pathway on EC, TNF-alpha stimulated an LFA-1-dependent/ICAM-1-dependent adhesion pathway on EC. In contrast, VLA-4/VCAM-1 molecules were involved in PBL adhesion both to IL-4 and to TNF-alpha-stimulated EC. Finally, we found that a CD2-dependent/LFA-3-independent adhesion pathway was mainly involved in IL-4-stimulated EC.

摘要

我们证明,肿瘤坏死因子α(TNF-α)和白细胞介素4(IL-4)通过促进转录和蛋白质合成来增加内皮细胞(EC)对外周血淋巴细胞(PBL)的黏附性。TNF-α和IL-4所观察到的不同动力学表明不同黏附分子的参与。阻断黏附试验和免疫荧光分析表明,PBL与内皮细胞的黏附涉及不同的配对黏附分子。虽然IL-4在EC上促进了一条依赖淋巴细胞功能相关抗原-1(LFA-1)/不依赖细胞间黏附分子-1(ICAM-1)的黏附途径,但TNF-α在EC上刺激了一条依赖LFA-1/依赖ICAM-1的黏附途径。相比之下,极迟抗原-4(VLA-4)/血管细胞黏附分子-1(VCAM-1)分子参与了PBL对IL-4和TNF-α刺激的EC的黏附。最后,我们发现一条依赖CD2/不依赖淋巴细胞功能相关抗原-3(LFA-3)的黏附途径主要参与了IL-4刺激的EC。

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