期刊
JOURNAL OF VIROLOGY
卷 88, 期 16, 页码 9350-9360出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00818-14
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资金
- U.S. National Institutes of Health [R01AI090059, R01ES015050, P42ES013648]
Respiratory syncytial virus (RSV) infection is the number one cause of bronchiolitis in infants, yet no vaccines are available because of a lack of knowledge of the infant immune system. Using a neonatal mouse model, we previously revealed that mice initially infected with RSV as neonates develop Th2-biased immunopathophysiologies during reinfection, and we demonstrated a role for enhanced interleukin-4 receptor alpha (IL-4R alpha) expression on T helper cells in these responses. Here we show that RSV infection in neonates induced limited type I interferon (IFN) and plasmacytoid dendritic cell (pDC) responses. IFN alpha (IFN-alpha) treatment or adoptive transfer of adult pDCs capable of inducing IFN-alpha prior to neonatal RSV infection decreased Th2-biased immunopathogenesis during reinfection. A reduced viral load and downregulation of IL-4R alpha on Th2 cells were observed in IFN-alpha -treated neonatal mice, suggesting dual mechanisms of action.
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