B cell flow cytometry data (FlowJo + FCS files) from the NIH/CHI influenza vaccination study
datasetposted on 23.02.2020, 05:17 by Yuri Kotliarov, Angélique Biancotto, Meghali Goswami, Foo Cheung, Pamela L Schwartzberg, John Tsang
PBMC sample collection and processing are described in Tsang, J. S. et al. Global analyses of human immune variation reveal baseline predictors of postvaccination responses. Cell 157, 499–513 (2014).
Additional B cell subpopulations were gated for the publication "Broad immune activation underlies shared set point signatures for vaccine responsiveness in healthy individuals and disease activity in patients with lupus". (Kotliarov Y, Sparks R et al. Nature Medicine 2020). These new gates include the CD20+CD38++ cells whose frequency evaluated prior to vaccination was predictive of antibody responses to vaccination.
This item is a part of the collection: https://doi.org/10.35092/yhjc.c.4753772
If you use our data (including CITE-seq data) or code for your work please cite the following publication:
Kotliarov, Y., Sparks, R. et al. Broad immune activation underlies shared set point signatures for vaccine responsiveness in healthy individuals and disease activity in patients with lupus. Nat. Med. DOI: https://doi.org/10.1038/s41591-020-0769-8 (2020)
Responses to vaccination and to diseases vary widely across individuals, which may be partly due to baseline immune variations. Identifying such baseline predictors and their biological basis are of broad interest given their potential importance for cancer immunotherapy, disease outcomes, vaccination and infection responses. Here we uncover baseline blood transcriptional signatures predictive of antibody responses to both influenza and yellow fever vaccinations in healthy subjects. These same signatures evaluated at clinical quiescence are correlated with disease activity in systemic lupus erythematosus patients with plasmablast-associated flares. CITE-seq profiling of 82 surface proteins and transcriptomes of 53,201 single cells from healthy high and low influenza-vaccination responders revealed that our signatures reflect the extent of activation in a plasmacytoid dendritic cell—Type I IFN—T/B lymphocyte network. Our findings raise the prospect that modulating such immune baseline states may improve vaccine responsiveness and mitigate undesirable autoimmune disease activities.
General contact: John Tsang (email@example.com)
Questions about software/code: Yuri Kotliarov (firstname.lastname@example.org)
Funded by the Intramural Research Program of the National Institute of Allergy and Infectious Diseases (NIAID) and NIH Institutes supporting the Center for Human Immunology (CHI), National Institutes of Health, Bethesda, MD, USA
1ZICAI001226 (NIH CHI)
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- AI - National Institute of Allergy and Infectious Diseases (NIAID)