TLR induces reorganization of the IgM-BCR complex regulating murine B-1 cell responses to infections.

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ID: 27313
2019
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Abstract
In mice, neonatally-developing, self-reactive B-1 cells generate steady levels of natural antibodies throughout life. B-1 cells can, however, also rapidly respond to infections with increased local antibody production. The mechanisms regulating these two seemingly very distinct functions are poorly understood, but have been linked to expression of CD5, an inhibitor of BCR-signaling. Here we demonstrate that TLR-mediated activation of CD5+ B-1 cells induced the rapid reorganization of the IgM-BCR complex, leading to the eventual loss of CD5 expression, and a concomitant increase in BCR-downstream signaling, both in vitro and in vivo after infections of mice with influenza virus and Both, initial CD5 expression and TLR-mediated stimulation, were required for the differentiation of B-1 cells to IgM-producing plasmablasts after infections. Thus, TLR-mediated signals support participation of B-1 cells in immune defense via BCR-complex reorganization.
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savage2019tlrelife Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Savage, Hannah P;Kläsener, Kathrin;Smith, Fauna L;Luo, Zheng;Reth, Michael;Baumgarth, Nicole;
Journal eLife
Year 2019
DOI
10.7554/eLife.46997
URL
Keywords Keywords not found

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