Duff G W, Durum S K
Yale J Biol Med. 1982 Sep-Dec;55(5-6):437-42.
The role of fever in host defense, if indeed it has one, is poorly understood. Fever in response to exogenous agents is mediated by a host macrophage product called endogenous pyrogen (EP). Recently it has been shown that EP is probably identical to interleukin 1 (IL1), an immunostimulatory macrophage product that induces T-cell proliferation. We postulated that the pyrogenic and immunostimulatory actions of this host mediator might be interrelated and tested T-cell proliferation induced by IL1 at a temperature characteristic of fever. The T-cell proliferative response to IL1 (and to the lymphokine, interleukin 2) was greatly increased at 39 degrees C compared to 37 degrees C, while B-cell mitogenesis in response to lipopolysaccharide was not. These findings suggest that, if similar events occur in vivo, fever may have important immunoregulatory significance and call into question the current indiscriminate use of antipyretic agents.
发热在宿主防御中的作用(如果确实存在的话),目前还知之甚少。对外源病原体产生的发热反应是由一种名为内源性致热原(EP)的宿主巨噬细胞产物介导的。最近有研究表明,EP可能与白细胞介素1(IL1)相同,IL1是一种免疫刺激巨噬细胞产物,可诱导T细胞增殖。我们推测这种宿主介质的致热作用和免疫刺激作用可能相互关联,并在发热特征温度下测试了IL1诱导的T细胞增殖。与37摄氏度相比,在39摄氏度时,T细胞对IL1(以及对淋巴因子白细胞介素2)的增殖反应大大增强,而B细胞对脂多糖的有丝分裂反应则没有变化。这些发现表明,如果体内发生类似事件,发热可能具有重要的免疫调节意义,并对目前不加区分地使用退热药提出了质疑。