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- W1559939892 abstract "Abstract Vitamin A deficiency (VAD) is a leading contributor to pediatric morbidity and mortality worldwide. Recently we have shown that VAD in mice impairs mucosal IgA responses in the upper respiratory tract during both paramyxovirus and influenza virus vaccination, thus impeding a first defense against these pathogens at their point of entry. The key vitamin A metabolite responsible for normal immune function is retinoic acid (RA). Previously, RA was believed to be produced predominantly by gut dendritic cells expressing aldehyde dehydrogenase (ALDH1A), an enzyme required for metabolism of RA from RA precursors. However, we found that epithelial cells of the respiratory tract autonomously produce ALDH1A. These cells also produce IL-6 and GM-CSF and can facilitate IgA production from activated splenocytes in vitro. Further in vitro analyses demonstrated that outcomes of vitamin A supplementation were affected by a variety of factors including concentration and type of vitamin A metabolite, as well as cells targeted. Based on these results, we supplemented a respiratory virus vaccine with a single intranasal dose of retinol, retinyl palmitate, or a combination of IL-6 and GM-CSF in VAD mice, and observed enhanced virus-specific mucosal IgA. In total, our data provide insight into the role of vitamin A in virus-specific immunity, while defining feasible methods for the correction of impaired mucosal immune responses in individuals with VAD." @default.
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- W1559939892 date "2014-05-01" @default.
- W1559939892 modified "2023-10-16" @default.
- W1559939892 title "Deciphering and correcting impaired respiratory virus-specific immunity caused by vitamin A deficiency (VIR2P.1017)" @default.
- W1559939892 doi "https://doi.org/10.4049/jimmunol.192.supp.75.6" @default.
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