Yoshinaga M
Kumamoto University Medical School, Japan.
Chin Med Sci J. 1991 Mar;6(1):36-40.
In order to shed some light on the mechanism by which inflammation modulates the immune response, the kinetics of IL-1 production and of the cells producing it as well as the control mechanisms involved were studied in a variety of animal models. In the case of casein-induced peritoneal inflammation in rabbits, IL-1 beta mRNA expression was found to be limited to the early stage--peaking at 2 h and lasting for only 5 h, a period corresponding to that in which new antigen introduction induces an enhanced immune response. This suggests that IL-1 beta is an inflammation-induced immune potentiation factor. Among 5-h peritoneal exudate cells (PEC) staining with anti-rabbit-IL-1 beta goat antibody, 99% were PMNs. Surprisingly, 9-h and 16-h PECs, which display negative IL-1 activity, also stained for IL-1 beta antigen. This seemingly contradictory data can be explained by the existence of a hypothetical processing protease subject to limited activation, and by a newly isolated 13 kD IL-1 antagonist produced during the later stages of inflammation.
为了深入了解炎症调节免疫反应的机制，我们在多种动物模型中研究了白细胞介素-1（IL-1）的产生动力学、产生IL-1的细胞以及相关的控制机制。在兔酪蛋白诱导的腹膜炎模型中，发现IL-1βmRNA表达仅限于早期阶段，在2小时达到峰值，仅持续5小时，这一时期与新抗原引入诱导增强免疫反应的时期相对应。这表明IL-1β是一种炎症诱导的免疫增强因子。在用抗兔IL-1β山羊抗体染色的5小时腹膜渗出细胞（PEC）中，99%为中性粒细胞。令人惊讶的是，显示阴性IL-1活性的9小时和16小时PEC也被染为IL-1β抗原阳性。这种看似矛盾的数据可以通过存在一种受有限激活的假设性加工蛋白酶，以及炎症后期新分离出的13 kD IL-1拮抗剂来解释。
