Gallucci S, Matzinger P
Ghost Laboratory, Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 4, Room 111, Bethesda, MD 20892, USA.
Curr Opin Immunol. 2001 Feb;13(1):114-9. doi: 10.1016/s0952-7915(00)00191-6.
The activation of dendritic cells, necessary for the initiation of primary and secondary immune responses, can be induced by endogenous danger signals - released by tissues undergoing stress, damage or abnormal death - and also by exogenous danger signals elaborated by pathogens. Some endogenous danger signals that recently have been discovered are heat-shock proteins, nucleotides, reactive oxygen intermediates, extracellular-matrix breakdown products, neuromediators and cytokines like the IFNs. We propose that allergy may be initiated by the direct damage of dendritic or other cells by toxic chemicals and allergenic proteases, and suggest that the triggering of danger signal receptors by exogenous pathogen-derived molecules may be more to the advantage of the pathogen than to the host.
树突状细胞的激活是启动初次和二次免疫反应所必需的,它可由内源性危险信号——由经历应激、损伤或异常死亡的组织释放——以及病原体产生的外源性危险信号诱导。最近发现的一些内源性危险信号包括热休克蛋白、核苷酸、活性氧中间体、细胞外基质降解产物、神经介质以及如干扰素等细胞因子。我们提出,过敏可能是由有毒化学物质和变应原蛋白酶对树突状细胞或其他细胞的直接损伤引发的,并表明外源性病原体衍生分子触发危险信号受体对病原体的益处可能大于对宿主的益处。