Espevik T, Brockhaus M, Loetscher H, Nonstad U, Shalaby R
Institute of Cancer Research, University of Trondheim, Norway.
J Exp Med. 1990 Feb 1;171(2):415-26. doi: 10.1084/jem.171.2.415.
Three different antibodies against a human TNF receptor (htr-1, htr-5, and htr-9) have been examined for their binding pattern to U937 cells and ability to mimic TNF-alpha activity in U937 cells, Fs4 fibroblasts, and human endothelial cells. Flow cytometric analysis revealed that htr-5 and htr-9 bound specifically to a TNF receptor on U937 cells that could be blocked by pretreatment with rTNF-alpha. Pretreatment of U937 cells with rTNF-beta blocked the binding of htr-9, but to a lesser extent htr-5 binding. Pretreatment with htr-5 inhibited the binding of htr-9 to U937 cells while pretreatment with htr-9 did not inhibit htr-5 binding. These results indicate that htr-5 and htr-9 recognize distinct but overlapping epitopes of a human TNF receptor on U937 cells and that htr-5 may be close to a TNF-alpha-specific domain of the binding site. Pretreatment with htr-5 or htr-9 only minimally reduced binding of BrTNF-alpha to U937 cells; however, these antibodies were much more effective in inhibiting BrTNF-alpha binding to HL-60 cells. Furthermore, it was found that htr-1 and htr-9, but not htr-5, had TNF-alpha activity on U937 cells, Fs4 fibroblasts, and endothelial cells and that the TNF-alpha activity induced by htr-9 was completely inhibited by htr-5. However, the cytotoxic activity of TNF-alpha was only partially inhibited by htr-5 on U937 cells while htr-5 had no effect on TNF-alpha activity on Fs4 cells. The data suggest that a common epitope is involved in inducing TNF-alpha activity in three different cell systems.
针对人肿瘤坏死因子受体(htr - 1、htr - 5和htr - 9)的三种不同抗体,已对其与U937细胞的结合模式以及在U937细胞、Fs4成纤维细胞和人内皮细胞中模拟肿瘤坏死因子α(TNF - α)活性的能力进行了检测。流式细胞术分析显示,htr - 5和htr - 9特异性结合U937细胞上的一种肿瘤坏死因子受体,该结合可被重组TNF - α预处理所阻断。用重组TNF - β预处理U937细胞可阻断htr - 9的结合,但对htr - 5结合的阻断程度较小。用htr - 5预处理可抑制htr - 9与U937细胞的结合,而用htr - 9预处理则不抑制htr - 5的结合。这些结果表明,htr - 5和htr - 9识别U937细胞上人肿瘤坏死因子受体的不同但重叠的表位,并且htr - 5可能靠近结合位点的TNF - α特异性结构域。用htr - 5或htr - 9预处理仅轻微降低生物活性TNF - α与U937细胞的结合;然而,这些抗体在抑制生物活性TNF - α与HL - 60细胞的结合方面更有效。此外,发现htr - 1和htr - 9,但不是htr - 5,在U937细胞、Fs4成纤维细胞和内皮细胞上具有TNF - α活性,并且htr - 9诱导的TNF - α活性被htr - 5完全抑制。然而,TNF - α的细胞毒性活性在U937细胞上仅被htr - 5部分抑制,而htr - 5对Fs4细胞上的TNF - α活性没有影响。数据表明,一个共同的表位参与在三种不同细胞系统中诱导TNF - α活性。