autocrine regulation of pulmonary inflammation by effector t-cell derived il-10 during infection with respiratory syncytial virus自分泌调节肺部炎症效应t细胞产生il - 10在呼吸道合胞病毒感染.pdf

Autocrine Regulation of Pulmonary Inflammation by Effector T-Cell Derived IL-10 during Infection with Respiratory Syncytial Virus 1 1 2 2 3 ¨ 4 Jie Sun , Amber Cardani , Ashish K. Sharma , Victor E. Laubach , Robert S. Jack , Werner Muller , Thomas J. Braciale1,5,6* 1The Beirne B. Carter Center for Immunology Research, The University of Virginia, Charlottesville, Virginia, United States of America, 2 Department of Surgery, The University of Virginia, Charlottesville, Virginia, United States of America, 3 Department of Immunology, University of Greifswald, Germany, 4 Bill Ford Chair of Cellular Immunology, Faculty of Life Sciences, University of Manchester, Manchester, United Kingdom, 5 Department of Microbiology, The University of Virginia, Charlottesville, Virginia, United States of America, 6 Department of Pathology, The University of Virginia, Charlottesville, Virginia, United States of America Abstract Respiratory syncytial virus (RSV) infection is the leading viral cause of severe lower respiratory tract illness in young infants. Clinical studies have documented that certain polymorphisms in the gene encoding the regulatory cytokine IL-10 are associated with the development of severe bronchiolitis in RSV infected infants. Here, we examined the role of IL-10 in a murine model of primary RSV infection and found that high levels of IL-10 are produced in the respiratory tract by anti-viral effector T cells at the onset of the adaptive immune response. We demonstrated that the function of the effector T cell - derived IL-10 in vivo is to limit the excess pulmonary inflammation and thereby to maintain critic