Department of Biochemistry, University of Lausanne, 155 Ch. Des Boveresses, Epalinges 1066, Switzerland.
Curr Opin Immunol. 2011 Feb;23(1):35-40. doi: 10.1016/j.coi.2010.10.016. Epub 2010 Nov 18.
The innate immune system has evolved the capacity to detect specific pathogens and to interrogate cell and tissue integrity in order to mount an appropriate immune response. Loss of homeostasis in the endoplasmic reticulum (ER) triggers the ER-stress response, a hallmark of many inflammatory and infectious diseases. The IRE1/XBP1 branch of the ER-stress signaling pathway has been recently shown to regulate and be regulated by innate immune signaling pathways in both the presence and absence of ER-stress. By contrast, innate immune pathways negatively affect the activation of two other branches of the ER-stress response as evidenced by reduced expression of the pro-apoptotic transcription factor CHOP. Here we will discuss how innate immune pathways and ER-signaling intersect to regulate the intensity and duration of innate immune responses.
先天免疫系统已经进化出了检测特定病原体和检查细胞和组织完整性的能力，以便引发适当的免疫反应。内质网 (ER) 中的内稳态丧失会触发 ER 应激反应，这是许多炎症和感染性疾病的标志。最近的研究表明，内质网应激信号通路的 IRE1/XBP1 分支在存在和不存在内质网应激的情况下，都可以被先天免疫信号通路所调节和调控。相比之下，先天免疫途径会对 ER 应激反应的另外两个分支的激活产生负面影响，证据是促凋亡转录因子 CHOP 的表达减少。在这里，我们将讨论先天免疫途径和 ER 信号之间如何相互作用，以调节先天免疫反应的强度和持续时间。
