Distinction of the memory B cell response to cognate antigen versus bystander inflammatory signals Academic Article uri icon

Overview

MeSH Major

  • Antigens
  • B-Lymphocytes
  • Bystander Effect
  • Cell Differentiation
  • Immunologic Memory
  • Inflammation

abstract

  • 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.

publication date

  • August 31, 2009

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2737154

Digital Object Identifier (DOI)

  • 10.1084/jem.20090667

PubMed ID

  • 19703988

Additional Document Info

start page

  • 2013

end page

  • 25

volume

  • 206

number

  • 9