Wang Jennifer P, Kurt-Jones Evelyn A, Shin Ok S, Manchak Michael D, Levin Myron J, Finberg Robert W
Department of Medicine, University of Massachusetts Medical Center, Worcester, 01605, USA.
J Virol. 2005 Oct;79(20):12658-66. doi: 10.1128/JVI.79.20.12658-12666.2005.
The pattern recognition receptor Toll-like receptor 2 (TLR2) has been implicated in the response to several human viruses, including herpes simplex viruses (types 1 and 2) and cytomegalovirus. We demonstrated that varicella-zoster virus (VZV) activates inflammatory cytokine responses via TLR2. VZV specifically induced interleukin-6 (IL-6) in human monocytes via TLR2-dependent activation of NF-kappaB, and small interfering RNA designed to suppress TLR2 mRNA reduced the IL-6 response to VZV in human monocyte-derived macrophages. Unlike other herpesviruses, the cytokine response to VZV was species specific. VZV did not induce cytokines in murine embryonic fibroblasts or in a mouse cell line, although VZV did activate NF-kappaB in a human cell line expressing a murine TLR2 construct. Together, these results suggest that TLR2 may play a role in the inflammatory response to VZV infection.
模式识别受体Toll样受体2（TLR2）与人体对多种病毒的反应有关，包括单纯疱疹病毒（1型和2型）和巨细胞病毒。我们证明水痘带状疱疹病毒（VZV）通过TLR2激活炎性细胞因子反应。VZV通过依赖TLR2的NF-κB激活在人单核细胞中特异性诱导白细胞介素-6（IL-6），设计用于抑制TLR2 mRNA的小干扰RNA降低了人单核细胞衍生巨噬细胞中对VZV的IL-6反应。与其他疱疹病毒不同，对VZV的细胞因子反应具有物种特异性。VZV在小鼠胚胎成纤维细胞或小鼠细胞系中不诱导细胞因子，尽管VZV在表达鼠TLR2构建体的人细胞系中确实激活了NF-κB。这些结果共同表明，TLR2可能在对VZV感染的炎症反应中发挥作用。
