Kappel M, Diamant M, Hansen M B, Klokker M, Pedersen B K
Department of Infectious Diseases M, Rigshospitalet, Copenhagen, Denmark.
Immunology. 1991 Jul;73(3):304-8.
The role of endogenously mediated fever and exogenous hyperthermia as modulators of immune functions remains poorly understood. It is known that fever is mediated by several cytokines, including interleukin-1 alpha and interleukin-1 beta (IL-1 alpha and IL-1 beta), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and the interferons. The present communication examines the effect of exogenous hyperthermia on the detection of these cytokines and shows the suppressive effect of elevated temperature (39 degrees) on the amount of IL-1 beta, IL-6 and IFN-gamma (P less than 0.001) but not on IL-1 alpha and TNF-alpha concentrations. It is suggested that a negative feedback mechanism exists between temperature and the production of some of the molecules involved in the mediation of fever. It is known that hyperthermia increases the proliferative response of lymphocytes. We found a twofold increase in [3H]thymidine incorporation at 39 degrees compared to 37 degrees. The distribution of cells expressing CD3, CD4, CD8, CD14, CD16, CD19 and CD25 markers was the same at 37 degrees and 39 degrees.
内源性介导的发热和外源性体温过高作为免疫功能调节因子的作用仍未得到充分了解。已知发热由多种细胞因子介导,包括白细胞介素-1α和白细胞介素-1β(IL-1α和IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和干扰素。本通讯研究了外源性体温过高对这些细胞因子检测的影响,并显示体温升高(39摄氏度)对IL-1β、IL-6和干扰素-γ的量有抑制作用(P<0.001),但对IL-1α和TNF-α浓度没有影响。提示温度与发热介导过程中一些相关分子的产生之间存在负反馈机制。已知体温过高会增加淋巴细胞的增殖反应。我们发现,与37摄氏度相比,在39摄氏度时[3H]胸苷掺入量增加了两倍。在37摄氏度和39摄氏度时,表达CD3、CD4、CD8、CD14、CD16、CD19和CD25标志物的细胞分布相同。