Kozel T R
Department of Microbiology and Cell and Molecular Biology Program, University of Nevada, Reno 89557, USA.
Clin Microbiol Rev. 1996 Jan;9(1):34-46. doi: 10.1128/CMR.9.1.34.
Fungi have been studied as prototype activators of the complement cascade since the early 1900s. More recently, attention has focused on the role of the complement system in the pathogenesis of fungal infections. The interactions of Cryptococcus neoformans and Candida albicans with the complement system are the most widely characterized; however, all pathogenic fungi examined to date have the ability to initiate the complement cascade. The molecular mechanisms for initiation and regulation of the complement cascade differ from one fungus to another, most likely reflecting differences in the structure of the outer layers of the cell wall. The molecular bases for such differences remain to be identified. Studies of mycoses in experimental animals with induced or congenital deficiencies in the complement system demonstrate that complement is an important innate system for control of fungal infection. Contributions to host resistance include opsonization and generation of inflammatory mediators. Inflammation induced by chemotactic products of the complement system may contribute to the pathogenesis of some fungal infections.
自20世纪初以来，真菌一直被作为补体级联反应的原型激活剂进行研究。最近，人们的注意力集中在补体系统在真菌感染发病机制中的作用上。新型隐球菌和白色念珠菌与补体系统的相互作用得到了最广泛的描述；然而，迄今为止所检测的所有致病真菌都有启动补体级联反应的能力。补体级联反应的启动和调节的分子机制因真菌而异，很可能反映了细胞壁外层结构的差异。这种差异的分子基础仍有待确定。对补体系统诱导性或先天性缺陷的实验动物进行的真菌病研究表明，补体是控制真菌感染的重要先天性系统。对宿主抵抗力的贡献包括调理作用和炎症介质的产生。补体系统趋化产物诱导的炎症可能有助于某些真菌感染的发病机制。
