Yu Philipp
Institute of Immunology, Philipps-Universität Marburg, Marburg, Germany.
Immunol Rev. 2016 Jan;269(1):85-99. doi: 10.1111/imr.12371.
In the last 20 years research in Immunology underwent fundamental changes. Most importantly, the identification of the key role of innate immune pattern recognition receptors (PRRs) that recognize evolutionarily conserved molecular patterns on infectious pathogens. This results in priming of innate immune cells, which in turn activate and direct the adaptive immune response. Progress in innate immune recognition instigated the current working hypothesis, that recognition of endogenous ligands by PRRs results in innate immune cell activation (autoinflammation) or activation of adaptive cells, with self-reactive antigen receptors (autoimmunity). In particular, nucleic acid-sensing innate immune receptors seem to be prime candidates for a mechanistic understanding of autoreactive activation of the immune system. However, it remains uncertain what the actual source of nucleic acid ligands is and what other signals are needed to drive activation of autoreactive innate immune cells and break self-tolerance of the adaptive immune system. Here, I will review our present understanding about whether the infection with exogenous retroviruses or the reactivation of endogenous retroviruses might play an etiological role in certain autoimmune conditions of humans and murine experimental models.
在过去20年里，免疫学研究发生了根本性变化。最重要的是，识别出了先天性免疫模式识别受体（PRR）的关键作用，这些受体可识别传染性病原体上进化上保守的分子模式。这会引发先天性免疫细胞的启动，进而激活并指导适应性免疫反应。先天性免疫识别方面的进展催生了当前的工作假说，即PRR识别内源性配体可导致先天性免疫细胞激活（自身炎症）或激活具有自身反应性抗原受体的适应性细胞（自身免疫）。特别是，核酸感应先天性免疫受体似乎是从机制上理解免疫系统自身反应性激活的主要候选对象。然而，核酸配体的实际来源是什么，以及驱动自身反应性先天性免疫细胞激活并打破适应性免疫系统自身耐受性还需要哪些其他信号，仍然不确定。在此，我将综述我们目前对于外源性逆转录病毒感染或内源性逆转录病毒重新激活是否可能在人类某些自身免疫性疾病和小鼠实验模型中起病因学作用的理解。
