Trede N S, Tsytsykova A V, Chatila T, Goldfeld A E, Geha R S
Division of Immunology, Children's Hospital, Boston, MA 02115, USA.
J Immunol. 1995 Jul 15;155(2):902-8.
We have studied the transcriptional activation of the human TNF-alpha gene by the superantigen staphylococcal enterotoxin A (SEA) in the human premonocytic cell line THP-1. Nuclear proteins from SEA-stimulated THP-1 cells bound strongly to kappa 3, the most proximal of three putative NF-kappa B binding sites (kappa 1-kappa 3) found in the 5' regulatory region of the TNF-alpha gene, but only weakly to kappa 1, the most distal of the NF-kappa B binding sites, and showed no binding to kappa 2. The mobility of the kappa 3-nucleoprotein complex was identical to that of complexes formed between nuclear proteins and the consensus NF-kappa B seuqence. Moreover, both 5' and 3' mutants of kappa 3 were unable to displace kappa 3 binding, suggesting that the kappa 3 binding complex induced by SEA has the characteristics of NF-kappa B. Studies using Abs directed against the NF-kappa B subunits p50 and p65 suggested that both p50 and p65 bind to the kappa 3 sequence. Reporter gene assays showed that deletion of kappa 3 (-99 to -89 bp) and point mutation of the three 5' guanine bases in the kappa 3 sequence reduced the inducibility of the TNF-alpha promoter by SEA and LPS. These results indicate that superantigen induces NF-kappa B in human monocytic cells and suggest that binding of NF-kappa B to the kappa 3 site of the TNF-alpha promoter plays an important role in the transcriptional activation of the TNF-alpha gene by superantigen.
我们研究了超抗原葡萄球菌肠毒素A(SEA)对人早幼单核细胞系THP-1中人肿瘤坏死因子-α(TNF-α)基因的转录激活作用。SEA刺激的THP-1细胞的核蛋白与κ3强烈结合,κ3是在TNF-α基因5'调控区发现的三个假定的核因子-κB(NF-κB)结合位点(κ1-κ3)中最靠近近端的位点,但与NF-κB结合位点中最远端的κ1结合较弱,且与κ2无结合。κ3-核蛋白复合物的迁移率与核蛋白和共有NF-κB序列形成的复合物相同。此外,κ3的5'和3'突变体均不能取代κ3结合,这表明SEA诱导的κ3结合复合物具有NF-κB的特征。使用针对NF-κB亚基p50和p65的抗体进行的研究表明,p50和p65均与κ3序列结合。报告基因分析显示,κ3缺失(-99至-89 bp)以及κ3序列中三个5'鸟嘌呤碱基的点突变降低了SEA和脂多糖(LPS)对TNF-α启动子的诱导能力。这些结果表明,超抗原在人单核细胞中诱导NF-κB,提示NF-κB与TNF-α启动子的κ3位点结合在超抗原对TNF-α基因的转录激活中起重要作用。