Limited Type I Interferons and Plasmacytoid Dendritic Cells during Neonatal Respiratory Syncytial Virus Infection Permit Immunopathogenesis upon Reinfection

作者：Cormier, Stephania A.; Shrestha, Bishwas; Saravia, Jordy; Lee, Greg I.; Shen, Li; DeVincenzo, John P.; Kim, Young-In; You, Dahui^*

来源：Journal of Virology, 2014, 88(16): 9350-9360.

DOI：10.1128/JVI.00818-14

• VIRAL-INFECTION
• T-CELLS
• ALPHA
• BRONCHIOLITIS
• INFANTS
• DISEASE
• INTERLEUKIN-4
• ASSOCIATION
• IL-4R-ALPHA
• DETERMINES

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.

• 出版日期2014-8
• 单位湖南师范大学