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High-affinity memory B cells induced by SARS-CoV-2 infection produce more plasmablasts and atypical memory B cells than those primed by mRNA vaccines.

Authors
  • Pape, Kathryn A1
  • Dileepan, Thamotharampillai1
  • Kabage, Amanda J2
  • Kozysa, Daria2
  • Batres, Rodolfo3
  • Evert, Clayton2
  • Matson, Michael2
  • Lopez, Sharon2
  • Krueger, Peter D1
  • Graiziger, Carolyn2
  • Vaughn, Byron P2
  • Shmidt, Eugenia2
  • Rhein, Joshua3
  • Schacker, Timothy W3
  • Khoruts, Alexander4
  • Jenkins, Marc K5
  • 1 Department of Microbiology and Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA; Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
  • 2 Department of Medicine, Division of Gastroenterology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
  • 3 Department of Medicine, Division of Infectious Disease, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
  • 4 Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA; Department of Medicine, Division of Gastroenterology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
  • 5 Department of Microbiology and Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA; Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. Electronic address: [email protected]
Type
Published Article
Journal
Cell Reports
Publisher
Elsevier
Publication Date
Oct 12, 2021
Volume
37
Issue
2
Pages
109823–109823
Identifiers
DOI: 10.1016/j.celrep.2021.109823
PMID: 34610291
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Although both infections and vaccines induce memory B cell (MBC) populations that participate in secondary immune responses, the MBCs generated in each case can differ. Here, we compare SARS-CoV-2 spike receptor binding domain (S1-RBD)-specific primary MBCs that form in response to infection or a single mRNA vaccination. Both primary MBC populations have similar frequencies in the blood and respond to a second S1-RBD exposure by rapidly producing plasmablasts with an abundant immunoglobulin (Ig)A+ subset and secondary MBCs that are mostly IgG+ and cross-react with the B.1.351 variant. However, infection-induced primary MBCs have better antigen-binding capacity and generate more plasmablasts and secondary MBCs of the classical and atypical subsets than do vaccine-induced primary MBCs. Our results suggest that infection-induced primary MBCs have undergone more affinity maturation than vaccine-induced primary MBCs and produce more robust secondary responses. Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

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