rig-i mediates the co-induction of tumor necrosis factor and type i interferon elicited by myxoma virus in primary human macrophagesrig - i的co-induction介导肿瘤坏死因子和粘液瘤病毒引发的i型干扰素主要人类巨噬细胞.pdfVIP

RIG-I Mediates the Co-Induction of Tumor Necrosis Factor and Type I Interferon Elicited by Myxoma Virus in Primary Human Macrophages 1,2 1,2 1,2 3 4 4 Fuan Wang , Xiujuan Gao , John W. Barrett , Qing Shao , Eric Bartee , Mohamed R. Mohamed , 4 4 1,2 5 1,2 Masmudur Rahman , Steve Werden , Timothy Irvine , Jingxin Cao , Gregory A. Dekaban , Grant McFadden1,2,4* 1 BioTherapeutics Research Group, Robarts Research Institute, London, Ontario, Canada, 2 Department of Microbiology and Immunology, The University of Western Ontario, London, Ontario, Canada, 3 Department of Anatomy Cell Biology, The University of Western Ontario, London, Ontario, Canada, 4 Department of Molecular Genetics and Microbiology, College of Medicine, University of Florida, Gainesville, Florida, United States of America, 5 National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada Abstract The sensing of pathogen infection and subsequent triggering of innate immunity are key to controlling zoonotic infections. Myxoma virus (MV) is a cytoplasmic DNA poxvirus that in nature infects only rabbits. Our previous studies have shown that MV infection of primary mouse cells is restricted by virus-induced type I interferon (IFN). However, little is known about the innate sensor(s) involved in activating signaling pathways leading to cellular defense responses in primary human immune cells. Here, we show that the complete restriction of MV infection in the primary human fibroblasts requires both tumor necrosis factor (TNF) and type I IFN. We