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

Year: 2019

Type: article

Abstract: Neonatally-developing, self-reactive B-1 cells generate steady levels natural antibodies throughout life. They 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 with influenza virus and Salmonella typhimurium . 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.

Source: eLife

DOI: 10.7554/elife.46997

Authors: Hannah P. Savage, Kathrin Kläsener, Fauna L. Smith, Zheng Luo, Michael Reth, Nicole Baumgarth

Institutions: University of California, Davis, University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics

Language: English

Topic: T-cell and B-cell Immunology

Subfield: Immunology

Field: Immunology and Microbiology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $2,500

Funders: Deutsche Forschungsgemeinschaft, National Institutes of Health, University of California, Davis, National Cancer Institute, National Institute of Allergy and Infectious Diseases, National Center for Advancing Translational Sciences

OpenAlex ID: W2969221683