β干扰素增强兔内毒素发热的机制：肿瘤坏死因子（恶病质素）可能参与其中。
Mechanism of augmentation of endotoxin fever by beta interferon in rabbits: possible participation of tumor necrosis factor (cachectin).
作者信息
Kawasaki H, Moriyama M, Nariuchi H
机构信息
NRI Life Science, Kanagawa, Japan.
出版信息
Infect Immun. 1992 Mar;60(3):933-6. doi: 10.1128/iai.60.3.933-936.1992.
We analyzed the mechanism of the augmentation of endotoxin fever by human beta interferon (IFN) cross-reacting to rabbit cells in rabbits by using a purified rabbit tumor necrosis factor (RaTNF) and a monoclonal anti-RaTNF. The late peak of fever evoked by the injection with both endotoxin and HuIFN was suppressed when the animals were injected previously with anti-RaTNF. IFN also augmented the pyrogenicity of RaTNF in a synergistic manner in rabbits. The blood collected 2 h after the injection of RaTNF plus IFN contained a significant endogenous TNF activity, and the serum was shown to be pyrogenic. The endogenous pyrogen activity in the 2-h blood was heat stable (70 degrees C, 30 min) and was reduced by the in vitro treatment with anti-RaTNF. These results suggest that IFN augments the febrile response of rabbits to endotoxin by stimulating endogenous TNF-mediated TNF production to induce the late peak of fever.
我们通过使用纯化的兔肿瘤坏死因子（RaTNF）和单克隆抗RaTNF，分析了人β干扰素（IFN）与兔细胞交叉反应增强兔内毒素发热的机制。当动物预先注射抗RaTNF时，内毒素和HuIFN注射引起的发热晚期峰值受到抑制。IFN还以协同方式增强了兔体内RaTNF的致热活性。注射RaTNF加IFN后2小时采集的血液含有显著的内源性TNF活性，且血清显示具有致热性。2小时血液中的内源性致热活性热稳定（70℃，30分钟），并通过抗RaTNF的体外处理而降低。这些结果表明，IFN通过刺激内源性TNF介导的TNF产生来诱导发热晚期峰值，从而增强兔对内毒素的发热反应。
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