Russell S
Peter MacCallum Cancer Center, St Andrews Place, East Melbourne, VIC, Australia.
Tissue Antigens. 2004 Aug;64(2):111-8. doi: 10.1111/j.1399-0039.2004.00277.x.
In the last 10 years, the human cell-surface molecule, CD46, has evolved from 'just another complement regulator' to a receptor for a striking array of pathogens. CD46 not only protects cells from complement-mediated attack and facilitates infection by a large number of pathogens, but also exerts complex effects on cellular immune function. It has been proposed that CD46 links innate and adaptive immunity by affecting cellular immune function in response to complement binding, and the role of CD46 in the pathogenesis of many infectious pathogens is now the subject of intense investigation. So far, the flood of information that implicates CD46 in modifying a host response to measles, Neisseria, human herpes virus 6, and pathogens that activate complement has not yet been matched with a comprehensive understanding of the molecular mechanisms by which CD46 affects immune function. This review summarizes the evidence that points to a significant role for CD46 in a range of pathological processes and describes how CD46 might exert its effects by altering signal transduction and antigen presentation pathways.
在过去十年中,人类细胞表面分子CD46已从“仅仅是另一种补体调节因子”演变为一系列病原体的受体。CD46不仅保护细胞免受补体介导的攻击并促进大量病原体的感染,还对细胞免疫功能产生复杂影响。有人提出,CD46通过响应补体结合影响细胞免疫功能来连接先天免疫和适应性免疫,目前CD46在许多传染性病原体发病机制中的作用是深入研究的课题。到目前为止,大量表明CD46参与调节宿主对麻疹、奈瑟菌、人类疱疹病毒6以及激活补体的病原体反应的信息,尚未与对CD46影响免疫功能分子机制的全面理解相匹配。本综述总结了表明CD46在一系列病理过程中起重要作用的证据,并描述了CD46如何通过改变信号转导和抗原呈递途径发挥其作用。