| Literature DB >> 33044226 |
Zainab Rahil1,2, Rebecca Leylek2, Christian M Schürch1,2, Han Chen1,2, Zach Bjornson-Hooper1,2, Shannon R Christensen3, Pier Federico Gherardini4, Salil S Bhate1,2,5, Matthew H Spitzer6, Gabriela K Fragiadakis7, Nilanjan Mukherjee1,2, Nelson Kim1,2, Sizun Jiang1,2, Jennifer Yo8, Brice Gaudilliere9, Melton Affrime10, Bonnie Bock10, Scott E Hensley3, Juliana Idoyaga2, Nima Aghaeepour9, Kenneth Kim8, Garry P Nolan1,2, David R McIlwain1,2,10.
Abstract
Influenza is a significant cause of morbidity and mortality worldwide. Here we show changes in the abundance and activation states of more than 50 immune cell subsets in 35 individuals over 11 time points during human A/California/2009 (H1N1) virus challenge monitored using mass cytometry along with other clinical assessments. Peak change in monocyte, B cell, and T cell subset frequencies coincided with peak virus shedding, followed by marked activation of T and NK cells. Results led to the identification of CD38 as a critical regulator of plasmacytoid dendritic cell function in response to influenza virus. Machine learning using study-derived clinical parameters and single-cell data effectively classified and predicted susceptibility to infection. The coordinated immune cell dynamics defined in this study provide a framework for identifying novel correlates of protection in the evaluation of future influenza therapeutics.Entities:
Keywords: Adaptive immunity; Immunology; Infectious disease; Influenza; Innate immunity
Mesh：
Year: 2020 PMID： 33044226 PMCID： PMC7598057 DOI： 10.1172/JCI137265
Source DB: PubMed Journal: J Clin Invest ISSN： 0021-9738 Impact factor: 14.808