Galiana-Arnoux D, Imler J-L
UPR9022 CNRS, Institut de Biologie Moléculaire et Cellulaire, 15, rue René Descartes, Strasbourg, France.
Tissue Antigens. 2006 Apr;67(4):267-76. doi: 10.1111/j.1399-0039.2006.00583.x.
Viral infections are first detected by a set of innate immunity receptors that detect primary infections by pathogens, and trigger a transcriptional response. Among the induced target genes, type I interferons (IFNs) are central to the antiviral response of the host. The receptors and signaling pathways that mediate the strong induction of the synthesis of these cytokines have long remained elusive. In the past few years, Toll-like receptors (TLRs) emerged as important sensors of infections. Several TLRs participate in the recognition of virus infection, interacting in particular with viral nucleic acids. Upon activation, TLRs interact with different cytosolic adapter molecules and activate transcription factors of the nuclear factor-kappaB and IFN regulatory factor families that concur to mediate induction of IFN-alpha/beta and other inflammatory cytokines. In addition to the transmembrane TLRs, cytosolic helicases also detect viral nucleic acids, and trigger type I IFN synthesis.
病毒感染首先由一组天然免疫受体检测到，这些受体可检测病原体的初次感染，并触发转录反应。在诱导的靶基因中，I型干扰素（IFN）是宿主抗病毒反应的核心。长期以来，介导这些细胞因子合成强烈诱导的受体和信号通路一直难以捉摸。在过去几年中，Toll样受体（TLR）成为感染的重要传感器。几种TLR参与病毒感染的识别，特别是与病毒核酸相互作用。激活后，TLR与不同的胞质衔接分子相互作用，并激活核因子-κB和IFN调节因子家族的转录因子，这些转录因子共同介导IFN-α/β和其他炎性细胞因子的诱导。除了跨膜TLR外，胞质解旋酶也能检测病毒核酸，并触发I型IFN的合成。
