Tracey K J, Cerami A
Department of Neurosurgery, New York Hospital-Cornell University Medical Centér.
Curr Opin Immunol. 1989 Feb;1(3):454-61. doi: 10.1016/0952-7915(88)90026-x.
The studies reviewed here represent but a fraction of those published in the field last year, but they serve to illustrate two important points: (1) the cytokine network possesses enormous diversity of biological function, and (2) it is redundant, such that overlapping and synergistic effects are observed between many different cytokines. The impact of this system on the host is pervasive and readily amplifiable, and integrates the diverse responses to infectious disease which may be either beneficial, protecting against infection, or deleterious, causing tissue injury and death. The example of cachectin/TNF illustrates this type of scenario: during local infection or inflammation, low levels of cachectin/TNF act to enhance immune responsiveness, stimulate blood-vessel growth, increase energy mobilization, induce the release of other cytokines, and promote wound-healing; when overwhelming infection occurs, as in septicemia, large quantities of cachectin/TNF reach the circulation and cause shock, MSOF, and death; if a persisting infection develops and cachectin/TNF is chronically secreted, it mediates a state of cachexia which may be fatal. Future studies will undoubtedly advance our understanding of these effects, and that of the other cytokines. The development of novel therapies for inflammation, septic shock, and cachexia may be based on such advances.
此处回顾的研究仅占去年该领域发表研究的一小部分，但它们有助于阐明两个要点：（1）细胞因子网络具有极其多样的生物学功能，（2）它是冗余的，以至于在许多不同细胞因子之间观察到重叠和协同效应。该系统对宿主的影响广泛且易于放大，并整合了对传染病的多种反应，这些反应可能是有益的，可预防感染，也可能是有害的，会导致组织损伤和死亡。恶病质素/肿瘤坏死因子的例子就说明了这种情况：在局部感染或炎症期间，低水平的恶病质素/肿瘤坏死因子起到增强免疫反应性、刺激血管生长、增加能量动员、诱导其他细胞因子释放以及促进伤口愈合的作用；当发生严重感染时，如败血症，大量的恶病质素/肿瘤坏死因子进入循环系统，导致休克、多系统器官功能衰竭和死亡；如果持续感染发展且恶病质素/肿瘤坏死因子持续分泌，它会介导一种恶病质状态，这可能是致命的。未来的研究无疑将增进我们对这些效应以及其他细胞因子效应的理解。针对炎症、感染性休克和恶病质的新型疗法可能基于这些进展。
