Hattori A, Hayashi K, Kohno M
Department of Biology, Gifu Pharmaceutical University, Japan.
FEBS Lett. 1996 Jan 29;379(2):157-60. doi: 10.1016/0014-5793(95)01502-7.
The role of the two types of tumor necrosis factor (TNF) receptors, TNF-R1 and TNF-R2, in mediating the capacity of TNF to stimulate nerve growth factor (NGF) production in fibroblasts has been investigated. Although Swiss 3T3 cells express both the TNF-R1 and TNF-R2, an agonistic anti-TNF R1 antibody, but not an agonistic anti-TNF-R2 antibody, increases the NGF mRNA level and stimulates the production of NGF protein in the cells. Treatment of the cells with a combination of anti-TNF-R2 antibody and interleukin-1 beta (IL-1 beta) does not increase the NGF production induced by IL-1 beta alone, although TNF's activity to stimulate NGF production is markedly enhanced by IL-1 beta. Furthermore, simultaneous addition of the both antibodies does not increase the NGF production above that observed with the anti-TNF-R1 antibody, indicating that TNF-R1 alone mediates the TNF's activity to stimulate NGF production in fibroblasts.
研究了两种类型的肿瘤坏死因子（TNF）受体，即TNF-R1和TNF-R2，在介导TNF刺激成纤维细胞产生神经生长因子（NGF）能力方面的作用。尽管瑞士3T3细胞同时表达TNF-R1和TNF-R2，但一种激动性抗TNF-R1抗体而非激动性抗TNF-R2抗体可增加细胞中NGF mRNA水平并刺激NGF蛋白的产生。用抗TNF-R2抗体和白细胞介素-1β（IL-1β）联合处理细胞，并不会增加单独由IL-1β诱导的NGF产生，尽管IL-1β可显著增强TNF刺激NGF产生的活性。此外，同时添加两种抗体并不会使NGF产生量超过使用抗TNF-R1抗体时观察到的水平，这表明仅TNF-R1介导了TNF刺激成纤维细胞产生NGF的活性。
