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- W4313379024 abstract "Abstract Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract-associated hospitalizations in children under the age of 2. Acute RSV infection induces both Th1- and Th2-associated responses, with elevated airway hyperactivity being highly correlated with increased Th2-associated responses. However, the mechanism for induction of Th1 vs. Th2-associated responses following RSV infection is currently unknown. The inhibitory ligands PD-L1 and PD-L2 serve a critical role in the induction and regulation of Th1 and Th2-associated responses, respectively, during acute infections as well as asthma. Following acute RSV infection, lung epithelial cells upregulate PD-L1 within 24 hours post-infection (p.i.) with peak expression occurring at day 6 p.i.. Furthermore, both lung and mediastinal lymph node (MedLN) CD11c+ cDCs and pDCs upregulate PD-L1 expression early following RSV infection and retain increased PD-L1 expression throughout the course of infection. In contrast, PD-L2 expression is primarily restricted to CD11c+ cDCs. PD-L2 expression peaks at day 6 p.i. on both lung and MedLN CD11c+ cDCs, correlating with increased airway resistance following acute RSV infection. PD-L2-blockade early during RSV infection results in increased airway hyperactivity, whereas PD-L1-blockade exhibited no significant effect. These data suggest that PD-L2 plays a critical role in the regulation of RSV-induced immunopathology." @default.
- W4313379024 created "2023-01-06" @default.
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- W4313379024 date "2013-05-01" @default.
- W4313379024 modified "2023-09-27" @default.
- W4313379024 title "Critical role of PD-L2 in limiting pulmonary immunopathology during RSV infection (P6182)" @default.
- W4313379024 doi "https://doi.org/10.4049/jimmunol.190.supp.189.6" @default.
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