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J Clin Invest. 2019 Jan 2;129(1):93-105. doi: 10.1172/JCI121341. Epub 2018 Nov 19.

Spec-seq unveils transcriptional subpopulations of antibody-secreting cells following influenza vaccination.

Author information

1
The Committee on Immunology.
2
The Department of Medicine, Section of Rheumatology.
3
The Department of Pathology, Molecular Pathogenesis and Molecular Medicine, and.
4
The Department of Ecology and Evolution, The University of Chicago, Chicago, Illinois, USA.
5
Emory Vaccine Center, Emory University, Atlanta, Georgia, USA.
6
The Department of Biochemistry and Molecular Biophysics, The University of Chicago, Chicago, Illinois, USA.
7
Toyota Technological Institute at Chicago, Chicago, Illinois, USA.

Abstract

Vaccines are among the most effective public health tools for combating certain infectious diseases such as influenza. The role of the humoral immune system in vaccine-induced protection is widely appreciated; however, our understanding of how antibody specificities relate to B cell function remains limited due to the complexity of polyclonal antibody responses. To address this, we developed the Spec-seq framework, which allows for simultaneous monoclonal antibody (mAb) characterization and transcriptional profiling from the same single cell. Here, we present the first application of the Spec-seq framework, which we applied to human plasmablasts after influenza vaccination in order to characterize transcriptional differences governed by B cell receptor (BCR) isotype and vaccine reactivity. Our analysis did not find evidence of long-term transcriptional specialization between plasmablasts of different isotypes. However, we did find enhanced transcriptional similarity between clonally related B cells, as well as distinct transcriptional signatures ascribed by BCR vaccine recognition. These data suggest IgG and IgA vaccine-positive plasmablasts are largely similar, whereas IgA vaccine-negative cells appear to be transcriptionally distinct from conventional, terminally differentiated, antigen-induced peripheral blood plasmablasts.

KEYWORDS:

Adaptive immunity; B cells; Immunology; Influenza; Vaccines

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