Strukov A I
Arkh Patol. 1981;43(1):3-12.
Immune inflammation (II) arises on the basis of immunopathological mechanisms and acquires certain qualitative and quantitative features. It develops in a sensitized host following a specific immune response. Several kinds of II are to be distinguished differing from each other by the prevalence of disorders in cellular or humoral immunity, the pattern of the antigen, involvement in the response of immunoglobulins of different classes, complement components and a set of mediators. According to Sell's scheme, six immunopathological mechanisms are distinguished which underlie the development of early (like immediate type hypersensitivity) or late (like delayed type hypersensitivity) immune inflammation. Sometimes humoral and cellular mechanisms alternate in II which is reflected in the morphological picture of inflammation. This is illustrated by an example of the study of tissue inflammatory reactions in the synovial membrane in rheumatoid arthritis. Immune inflammation shows a trend to self-reproduction and continuous course with periods of remission and exacerbation of different durations. Timely recognition of immune inflammation is important both theoretically and practically.
免疫炎症(II)基于免疫病理机制产生,并具有一定的质和量的特征。它在致敏宿主中特定免疫反应后发生。几种免疫炎症可通过细胞免疫或体液免疫紊乱的普遍性、抗原模式、不同类别的免疫球蛋白、补体成分和一组介质参与反应的情况来区分。根据塞尔的方案,可区分出六种免疫病理机制,它们是早期(如速发型超敏反应)或晚期(如迟发型超敏反应)免疫炎症发展的基础。有时在免疫炎症中体液和细胞机制交替出现,这反映在炎症的形态学表现中。类风湿性关节炎滑膜组织炎症反应的研究实例说明了这一点。免疫炎症呈现出自复制和持续病程的趋势,伴有不同持续时间的缓解期和加重期。及时识别免疫炎症在理论和实践上都很重要。