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肿瘤坏死因子与白细胞介素-4或γ干扰素结合,以选择性增强内皮细胞对T细胞的黏附性。血管细胞黏附分子-1依赖性和非依赖性结合机制的作用。

Tumor necrosis factor combines with IL-4 or IFN-gamma to selectively enhance endothelial cell adhesiveness for T cells. The contribution of vascular cell adhesion molecule-1-dependent and -independent binding mechanisms.

作者信息

Thornhill M H, Wellicome S M, Mahiouz D L, Lanchbury J S, Kyan-Aung U, Haskard D O

机构信息

Division of Medicine, United Medical School, Guy's Hospital, London, England.

出版信息

J Immunol. 1991 Jan 15;146(2):592-8.

PMID:1702807
Abstract

The adhesion of lymphocytes to vascular endothelium is the first step in their passage from the blood into inflammatory tissues. By modulating endothelial cell (EC) adhesiveness for lymphocytes, cytokines may regulate lymphocyte accumulation and hence the nature and progression of inflammatory responses. IL-1, TNF, IFN-gamma, and IL-4 each increase EC adhesiveness for T cells when used alone in adhesion assays in vitro. As cytokines are more likely to act in combination at sites of inflammation in vivo, we have studied the stimulating effect of different combinations of cytokines on EC adhesiveness for T cells and polymorphonuclear leukocytes (PMN). Acting alone IL-1, TNF, IFN-gamma, and IL-4 each significantly enhanced EC adhesiveness for T cells (p less than 0.005), whereas only IL-1 (p less than 0.005) and TNF (p less than 0.005) but not IFN-gamma or IL-4 significantly enhanced adhesiveness for PMN. When EC were stimulated with optimal concentrations of TNF in combination with IL-4 or IFN-gamma, there was a significant further increase in adhesiveness for T cells (p less than 0.003), but not PMN, over that seen with TNF alone. The additive effect of TNF and IL-4 was more marked than that of TNF and IFN-gamma. Although approximately equal proportions of T cells and PMN bound to TNF-stimulated EC, nearly double the proportion of T cells compared with PMN bound EC preincubated with TNF and IL-4 together. A similar interaction with IL-4 or IFN-gamma was exhibited by lymphotoxin. mAb-inhibition studies indicated that the extra increase in binding caused by stimulating EC with TNF and IL-4 in combination was mediated by VCAM-1 whereas that caused by stimulating with TNF and IFN-gamma in combination was substantially mediated through leukocyte function-associated Ag-1- and VCAM-1-independent mechanisms. These observations suggest that whereas IL-1 and TNF alone are unselective in terms of leukocyte adhesion to EC, the combination of TNF (or LT) with IL-4 or IFN-gamma may be of key importance in determining the recruitment of a lymphocyte-predominant infiltrate in immune mediated inflammation, and in initiating the transition from acute to chronic inflammation.

摘要

淋巴细胞与血管内皮的黏附是其从血液进入炎症组织的第一步。细胞因子可通过调节内皮细胞(EC)对淋巴细胞的黏附性,来调控淋巴细胞的聚集,进而影响炎症反应的性质和进程。在体外黏附试验中,单独使用白细胞介素-1(IL-1)、肿瘤坏死因子(TNF)、γ干扰素(IFN-γ)和白细胞介素-4(IL-4)时,均可增加EC对T细胞的黏附性。由于细胞因子在体内炎症部位更可能以组合形式发挥作用,因此我们研究了不同细胞因子组合对EC与T细胞及多形核白细胞(PMN)黏附性的刺激作用。单独作用时,IL-1、TNF、IFN-γ和IL-4均可显著增强EC对T细胞的黏附性(p<0.005),而只有IL-1(p<0.005)和TNF(p<0.005)能显著增强对PMN的黏附性,IFN-γ和IL-4则无此作用。当用最佳浓度的TNF与IL-4或IFN-γ联合刺激EC时,与单独使用TNF相比,对T细胞的黏附性有显著进一步增加(p<0.003),但对PMN则无此作用。TNF与IL-4的相加作用比TNF与IFN-γ更明显。虽然与TNF刺激的EC结合的T细胞和PMN比例大致相等,但与TNF和IL-4共同预孵育的EC结合的T细胞比例几乎是PMN的两倍。淋巴毒素也表现出与IL-4或IFN-γ类似的相互作用。单克隆抗体抑制研究表明,TNF与IL-4联合刺激EC导致的结合额外增加是由血管细胞黏附分子-1(VCAM-1)介导的,而TNF与IFN-γ联合刺激导致的结合增加主要是通过白细胞功能相关抗原-1(leukocyte function-associated Ag-1)和不依赖VCAM-1的机制介导的。这些观察结果表明,虽然单独的IL-1和TNF在白细胞与EC的黏附方面没有选择性,但TNF(或淋巴毒素)与IL-4或IFN-γ的组合在决定免疫介导炎症中以淋巴细胞为主的浸润细胞募集以及启动从急性炎症向慢性炎症的转变方面可能至关重要。

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