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肿瘤坏死因子-α与白细胞介素-1的协同及重叠活性

Synergistic and overlapping activities of tumor necrosis factor-alpha and IL-1.

作者信息

Last-Barney K, Homon C A, Faanes R B, Merluzzi V J

机构信息

Department of Immunology, Boehringer Ingelheim Pharamaceuticals, Inc., Ridgefield, CT 06877.

出版信息

J Immunol. 1988 Jul 15;141(2):527-30.

PMID:3260255
Abstract

TNF-alpha and IL-1 induce the production of PGE2 from human chondrosarcoma, fibrosarcoma, and carcinoma cell lines. When combined at sub-optimal concentrations, TNF-alpha and IL-1 synergistically stimulate PGE2 production. The synergy of TNF-alpha and IL-1 on the induction of PGE2 is partially neutralized by specific antibodies. In vitro, human rTNF-alpha is directly cytotoxic to several human transplantable tumor cell lines. These include a human carcinoma, human chondrosarcoma, and a human transformed fibroblast cell line. The cytotoxic effect of TNF-alpha was abrogated by a specific, neutralizing, polyclonal antibody. IL-1 had no direct cytotoxic effect on these cell lines; however, IL-1 enhanced the cytotoxic effects of TNF-alpha. The synergy of these two cytokines in the cytotoxic assay was neutralized by the addition of specific neutralizing antibodies.

摘要

肿瘤坏死因子-α(TNF-α)和白细胞介素-1(IL-1)可诱导人软骨肉瘤、纤维肉瘤和癌细胞系产生前列腺素E2(PGE2)。当以次优浓度联合使用时,TNF-α和IL-1可协同刺激PGE2的产生。TNF-α和IL-1对PGE2诱导的协同作用可被特异性抗体部分中和。在体外,人重组TNF-α对几种人可移植肿瘤细胞系具有直接细胞毒性。这些细胞系包括人癌、人软骨肉瘤和人转化成纤维细胞系。TNF-α的细胞毒性作用可被一种特异性、中和性多克隆抗体消除。IL-1对这些细胞系没有直接细胞毒性作用;然而,IL-1增强了TNF-α的细胞毒性作用。在细胞毒性试验中,这两种细胞因子的协同作用可通过添加特异性中和抗体而被中和。

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