Fishman M, Larche M
Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38101-0318.
Cell Immunol. 1993 Dec;152(2):510-21. doi: 10.1006/cimm.1993.1308.
Receptor-dependent tumor necrosis factor (TNF)-mediated activities against mouse thymoma cells and normal thymocytes syngeneic for C57 mice were examined to determine the specific involvement of TNF receptors R1 and R2. Both receptors are expressed by EL4 thymoma cells and normal C57 thymocytes. TNF-mediated activities included (a) cytotoxicity, (b) induction of hyposensitivity to TNF-mediated lysis, (c) costimulatory stimulation of thymocyte proliferation, and (d) activation of NF-kB-like transcription factor. The ability of polyclonal antisera against TNF receptors to mimic the above TNF-mediated activities was determined. The results clearly showed that anti-TNF-R1 antibodies were cytotoxic against EL4 cells, induced hyposensitivity of S-EL4 to TNF lysis and activated the NF-kB-like transcription factor in EL 4 cells and syngeneic normal thymocytes. Antisera against TNF-R2 only mimicked TNF-mediated costimulation of thymocyte proliferation with IL2. No direct correlation was noted between TNF activation of NF-kB and TNF-mediated lysis.
研究了受体依赖性肿瘤坏死因子（TNF）介导的针对C57小鼠同基因的小鼠胸腺瘤细胞和正常胸腺细胞的活性，以确定TNF受体R1和R2的具体参与情况。两种受体均由EL4胸腺瘤细胞和正常C57胸腺细胞表达。TNF介导的活性包括：（a）细胞毒性；（b）诱导对TNF介导的裂解的低敏感性；（c）共刺激胸腺细胞增殖；以及（d）激活NF-κB样转录因子。测定了针对TNF受体的多克隆抗血清模拟上述TNF介导活性的能力。结果清楚地表明，抗TNF-R1抗体对EL4细胞具有细胞毒性，诱导S-EL4对TNF裂解的低敏感性，并激活EL4细胞和同基因正常胸腺细胞中的NF-κB样转录因子。抗TNF-R2抗血清仅模拟TNF介导的用IL2共刺激胸腺细胞增殖。未观察到TNF激活NF-κB与TNF介导的裂解之间有直接相关性。
