Errett John S, Gale Michael
Center for Innate Immunity and Immune Disease, Department of Immunology, School of Medicine, University of Washington, Seattle, 98109, USA.
Virol Sin. 2015 Jun;30(3):163-73. doi: 10.1007/s12250-015-3604-5. Epub 2015 May 20.
Innate immunity is critical for the control of virus infection and operates to restrict viral susceptibility and direct antiviral immunity for protection from acute or chronic viral-associated diseases including cancer. RIG-I like receptors (RLRs) are cytosolic RNA helicases that function as pathogen recognition receptors to detect RNA pathogen associated molecular patterns (PAMPs) of virus infection. The RLRs include RIG-I, MDA5, and LGP2. They function to recognize and bind to PAMP motifs within viral RNA in a process that directs the RLR to trigger downstream signaling cascades that induce innate immunity that controls viral replication and spread. Products of RLR signaling also serve to modulate the adaptive immune response to infection. Recent studies have additionally connected RLRs to signaling cascades that impart inflammatory and apoptotic responses to virus infection. Viral evasion of RLR signaling supports viral outgrowth and pathogenesis, including the onset of viral-associated cancer.
天然免疫对于控制病毒感染至关重要，其作用是限制病毒易感性并引导抗病毒免疫，以保护机体免受包括癌症在内的急性或慢性病毒相关疾病的侵害。视黄酸诱导基因I样受体（RLRs）是胞质RNA解旋酶，作为病原体识别受体发挥作用，以检测病毒感染的RNA病原体相关分子模式（PAMPs）。RLRs包括RIG-I、MDA5和LGP2。它们在识别并结合病毒RNA内的PAMP基序的过程中发挥作用，该过程引导RLR触发下游信号级联反应，从而诱导控制病毒复制和传播的天然免疫。RLR信号传导的产物还可调节对感染的适应性免疫反应。最近的研究还将RLRs与赋予病毒感染炎症和凋亡反应的信号级联联系起来。病毒对RLR信号传导的逃避支持病毒生长和发病机制，包括病毒相关癌症的发生。
