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Distinction of the memory B cell response to cognate antigen versus bystander inflammatory signals

The hypothesis that bystander inflammatory signals promote memory B cell (B(MEM)) self-renewal and differentiation in an antigen-independent manner is critically evaluated herein. To comprehensively address this hypothesis, a detailed analysis is presented examining the response profiles of B-2 line...

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Autores principales: Benson, Micah J., Elgueta, Raul, Schpero, William, Molloy, Michael, Zhang, Weijun, Usherwood, Edward, Noelle, Randolph J.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737154/
https://www.ncbi.nlm.nih.gov/pubmed/19703988
http://dx.doi.org/10.1084/jem.20090667
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author Benson, Micah J.
Elgueta, Raul
Schpero, William
Molloy, Michael
Zhang, Weijun
Usherwood, Edward
Noelle, Randolph J.
author_facet Benson, Micah J.
Elgueta, Raul
Schpero, William
Molloy, Michael
Zhang, Weijun
Usherwood, Edward
Noelle, Randolph J.
author_sort Benson, Micah J.
collection PubMed
description The hypothesis that bystander inflammatory signals promote memory B cell (B(MEM)) self-renewal and differentiation in an antigen-independent manner is critically evaluated herein. To comprehensively address this hypothesis, a detailed analysis is presented examining the response profiles of B-2 lineage B220(+)IgG(+) B(MEM) toward cognate protein antigen in comparison to bystander inflammatory signals. After in vivo antigen encounter, quiescent B(MEM) clonally expand. Surprisingly, proliferating B(MEM) do not acquire germinal center (GC) B cell markers before generating daughter B(MEM) and differentiating into plasma cells or form structurally identifiable GCs. In striking contrast to cognate antigen, inflammatory stimuli, including Toll-like receptor agonists or bystander T cell activation, fail to induce even low levels of B(MEM) proliferation or differentiation in vivo. Under the extreme conditions of adjuvanted protein vaccination or acute viral infection, no detectable bystander proliferation or differentiation of B(MEM) occurred. The absence of a B(MEM) response to nonspecific inflammatory signals clearly shows that B(MEM) proliferation and differentiation is a process tightly controlled by the availability of cognate antigen.
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spelling pubmed-27371542010-02-28 Distinction of the memory B cell response to cognate antigen versus bystander inflammatory signals Benson, Micah J. Elgueta, Raul Schpero, William Molloy, Michael Zhang, Weijun Usherwood, Edward Noelle, Randolph J. J Exp Med Article The hypothesis that bystander inflammatory signals promote memory B cell (B(MEM)) self-renewal and differentiation in an antigen-independent manner is critically evaluated herein. To comprehensively address this hypothesis, a detailed analysis is presented examining the response profiles of B-2 lineage B220(+)IgG(+) B(MEM) toward cognate protein antigen in comparison to bystander inflammatory signals. After in vivo antigen encounter, quiescent B(MEM) clonally expand. Surprisingly, proliferating B(MEM) do not acquire germinal center (GC) B cell markers before generating daughter B(MEM) and differentiating into plasma cells or form structurally identifiable GCs. In striking contrast to cognate antigen, inflammatory stimuli, including Toll-like receptor agonists or bystander T cell activation, fail to induce even low levels of B(MEM) proliferation or differentiation in vivo. Under the extreme conditions of adjuvanted protein vaccination or acute viral infection, no detectable bystander proliferation or differentiation of B(MEM) occurred. The absence of a B(MEM) response to nonspecific inflammatory signals clearly shows that B(MEM) proliferation and differentiation is a process tightly controlled by the availability of cognate antigen. The Rockefeller University Press 2009-08-31 /pmc/articles/PMC2737154/ /pubmed/19703988 http://dx.doi.org/10.1084/jem.20090667 Text en © 2009 Benson et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle Article
Benson, Micah J.
Elgueta, Raul
Schpero, William
Molloy, Michael
Zhang, Weijun
Usherwood, Edward
Noelle, Randolph J.
Distinction of the memory B cell response to cognate antigen versus bystander inflammatory signals
title Distinction of the memory B cell response to cognate antigen versus bystander inflammatory signals
title_full Distinction of the memory B cell response to cognate antigen versus bystander inflammatory signals
title_fullStr Distinction of the memory B cell response to cognate antigen versus bystander inflammatory signals
title_full_unstemmed Distinction of the memory B cell response to cognate antigen versus bystander inflammatory signals
title_short Distinction of the memory B cell response to cognate antigen versus bystander inflammatory signals
title_sort distinction of the memory b cell response to cognate antigen versus bystander inflammatory signals
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737154/
https://www.ncbi.nlm.nih.gov/pubmed/19703988
http://dx.doi.org/10.1084/jem.20090667
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