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- W90934187 abstract "Abstract Respiratory syncytial virus (RSV) infection accounts for significant morbidity in young infants. The survivors become susceptible to develop asthma later in life. Studies have shown increased airway responsiveness in these individuals and a concomitant Th2 response in their lungs. However, the underlying mechanism (s) responsible for this pulmonary Th2 response in post- RSV infection period is not well understood. In this study, using a mouse model, we examined whether differentiation of lung dendritic cells (DCs) was skewed due to RSV infection and whether a Th2 cytokine response was associated. Neonatal mice were sensitized with intraperitoneal ovalabumin (ova) and infected with intranasal RSV followed by subsequent challenge with intranasal ova. Flowcytometric analysis of lung parenchymal cells determined the proportions of CD11bloCD11chiCD45R- myeloid DCs (mDCs) and CD11blo CD11chi CD45Rhi plasmacytoid DCs (pDCs). An increase in the numbers of pDCs was observed in the lungs of RSV-infected as well as RSV-infected and ova-exposed mice. To mention, pDCs are reported to downregulate Th1 responses. Consistent to this, augmentation of Th2 cytokine responses was observed in the RSV-infected and ova-exposed mice. Thus, polarization of lung DCs towards pDC due to RSV infection may modulate lung cytokine responses leading to susceptibility to asthma in later life. Reversal or inhibition of this skewed polarization may be considered as a clinical strategy in the post-RSV infection asthma. In this connection, we have reported that GMCSF and IL4 treatment expands lung dendritic cell population with enhanced Th1 responses." @default.
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- W90934187 date "2007-04-01" @default.
- W90934187 modified "2023-09-26" @default.
- W90934187 title "Skewed polarization of pulmonary dendritic cells in RSV-infection and susceptibility to asthma (39.2)" @default.
- W90934187 doi "https://doi.org/10.4049/jimmunol.178.supp.39.2" @default.
- W90934187 hasPublicationYear "2007" @default.
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