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Toll样受体3(TLR3)作为病毒双链RNA识别受体在机体抗病毒天然免疫中发挥十分重要的作用。TLR3识别配体后通过含TIR结构域的转接蛋白(TRIF)途径活化转录因子NF-κB和干扰素调节因子3(IRF3),诱导炎症细胞释放炎症因子并介导炎症反应,同时诱导I型干扰素的释放,介导抗病毒天然免疫。在一些病毒感染中TLR3通过诱导组织损伤介导病毒的扩散从而加重疾病的严重程度。部分肿瘤细胞也表达TLR3,活化的TLR3介导细胞凋亡、抑制细胞增殖,提示TLR3可能是肿瘤免疫治疗的新靶点。
Toll-like receptor 3 (TLR3) as a viral double-stranded RNA recognition receptor plays a very important role in the natural antiviral innate immunity. TLR3 activates the transcription factor NF-κB and interferon regulatory factor 3 (IRF3) through TIR domain-containing adapter protein (TRIF) pathway to induce inflammatory cells to release inflammatory cytokines and mediate inflammatory responses while inducing type I The release of interferon mediates antiviral innate immunity. In some viral infections, TLR3 aggravates the severity of the disease by mediating the spread of the virus by inducing tissue damage. Some tumor cells also expressed TLR3, activated TLR3 mediated apoptosis, inhibited cell proliferation, suggesting that TLR3 may be a new target for tumor immunotherapy.