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Liver Is a Generative Site for the B Cell Response to Ehrlichia muris.

Authors
  • Trivedi, Nikita1
  • Weisel, Florian2
  • Smita, Shuchi3
  • Joachim, Stephen2
  • Kader, Muhamuda4
  • Radhakrishnan, Aditya5
  • Clouser, Chris5
  • Rosenfeld, Aaron M6
  • Chikina, Maria7
  • Vigneault, Francois5
  • Hershberg, Uri6
  • Ismail, Nahed4
  • Shlomchik, Mark Jay8
  • 1 Department of Immunology, University of Pittsburgh, Pittsburgh, PA 15261, USA; Graduate Program in Microbiology and Immunology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
  • 2 Department of Immunology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
  • 3 Department of Immunology, University of Pittsburgh, Pittsburgh, PA 15261, USA; Department of Computational and Systems Biology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
  • 4 Department of Pathology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
  • 5 Juno Therapeutics, Seattle, WA 98109, USA.
  • 6 Drexel University, Philadelphia, PA 19104, USA.
  • 7 Department of Computational and Systems Biology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
  • 8 Department of Immunology, University of Pittsburgh, Pittsburgh, PA 15261, USA. Electronic address: [email protected]
Type
Published Article
Journal
Immunity
Publication Date
Dec 17, 2019
Volume
51
Issue
6
Identifiers
DOI: 10.1016/j.immuni.2019.10.004
PMID: 31732168
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The B cell response to Ehrlichia muris is dominated by plasmablasts (PBs), with few-if any-germinal centers (GCs), yet it generates protective immunoglobulin M (IgM) memory B cells (MBCs) that express the transcription factor T-bet and harbor V-region mutations. Because Ehrlichia prominently infects the liver, we investigated the nature of liver B cell response and that of the spleen. B cells within infected livers proliferated and underwent somatic hypermutation (SHM). Vh-region sequencing revealed trafficking of clones between the spleen and liver and often subsequent local clonal expansion and intraparenchymal localization of T-bet+ MBCs. T-bet+ MBCs expressed MBC subset markers CD80 and PD-L2. Many T-bet+ MBCs lacked CD11b or CD11c expression but had marginal zone (MZ) B cell phenotypes and colonized the splenic MZ, revealing T-bet+ MBC plasticity. Hence, liver and spleen are generative sites of B cell responses, and they include V-region mutation and result in liver MBC localization. Copyright © 2019 Elsevier Inc. All rights reserved.

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