Department of Medicine, Immunology Institute, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, NY 10029, USA.
Curr Opin Immunol. 2010 Feb;22(1):55-62. doi: 10.1016/j.coi.2010.01.003.
While inflammatory phagocytosis of microbial pathogens and non-inflammatory phagocytosis of apoptotic cells have each been studied extensively, the consequences of innate immune recognition of host cells undergoing apoptosis as a direct result of infection are unclear. In this situation, the innate immune system is confronted with mixed signals, those from apoptotic cells and those from the infecting pathogen. Nuclear receptor activation has been implicated downstream of apoptotic cell recognition while Toll-like receptors are the prototypical inflammatory receptors engaged during infection. When the two signals combine, a new set of events takes place beginning with transrepression of a subset of inflammatory-response genes and ending with the induction of a T helper-17 adaptive immune response. This response is best suited for clearing the infecting pathogen and repairing the damage that occurred to the host tissue during infection.
虽然对微生物病原体的炎症性吞噬作用和对凋亡细胞的非炎症性吞噬作用都进行了广泛的研究，但宿主细胞在感染过程中直接发生凋亡时，先天免疫系统对其识别的后果尚不清楚。在这种情况下，先天免疫系统面临着混合信号，既有来自凋亡细胞的信号，也有来自感染病原体的信号。核受体的激活被认为是凋亡细胞识别的下游事件，而 Toll 样受体则是感染过程中典型的炎症受体。当这两种信号结合时，一系列新的事件开始发生，首先是一组炎症反应基因的转录抑制，最后是诱导辅助性 T 细胞 17（T helper-17，Th17）适应性免疫反应。这种反应最适合清除感染病原体并修复感染过程中宿主组织发生的损伤。
