Kluger M J, Kozak W, Leon L R, Soszynski D, Conn C A
Institute for Basic and Applied Medical Research, Lovelace Institutes, Albuquerque, N.Mex., USA.
Neuroimmunomodulation. 1995 Jul-Aug;2(4):216-23. doi: 10.1159/000097199.
Fever is an excellent example of neuroimmunomodulation in that mediators of immunity initiate a pathway to raise the thermoregulatory set-point, resulting in behavioral and physiological responses that increase body temperature. This rise in temperature is thought to be adaptive, facilitating host defenses. Many cytokines are endogenous mediators of fever (i.e. endogenous pyrogens), including interleukin (IL)-, 1 beta, IL-6 and others. Tumor necrosis factor-alpha may be both an endogenous pyrogen and an endogenous antipyretic or cryogen, depending on the nature of the inflammatory stimuli. Although there is evidence that cytokines within the hypothalamus initiate fever, recent findings indicate that the signal to increase these brain cytokines may be neural (i.e. from peripheral nerves), rather than humoral (i.e. circulating endogenous pyrogen).
发热是神经免疫调节的一个典型例子,即免疫介质启动一条途径来提高体温调节设定点,从而导致行为和生理反应,使体温升高。这种体温升高被认为是适应性的,有助于宿主防御。许多细胞因子是发热的内源性介质(即内源性致热原),包括白细胞介素(IL)-1β、IL-6等。肿瘤坏死因子-α可能既是内源性致热原,又是内源性解热剂或退热剂,这取决于炎症刺激的性质。虽然有证据表明下丘脑内的细胞因子引发发热,但最近的研究结果表明,增加这些脑内细胞因子的信号可能是神经源性的(即来自外周神经),而非体液性的(即循环内源性致热原)。