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Murine germinal center B cells require functional Fms-like tyrosine kinase 3 signaling for IgG1 class-switch recombination.

Journal article
Authors Mattias Svensson
Karin Andersson
Caroline Wasén
Malin Erlandsson
Merja Nurkkala Karlsson
Ing-Marie Jonsson
Mikael Brisslert
Mats Bemark
Maria Bokarewa
Published in Proceedings of the National Academy of Sciences of the United States of America
Volume 112
Issue 48
Pages E6644-53
ISSN 1091-6490
Publication year 2015
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Institute of Biomedicine, Department of Microbiology and Immunology
Pages E6644-53
Language en
Links dx.doi.org/10.1073/pnas.1514191112
Keywords Flt3, B cell, germinal center, IgG1
Subject categories Immunobiology

Abstract

Switched antibody classes are important for efficient immune responses. Aberrant antibody production to otherwise harmless antigens may result in autoimmunity. The protein kinase fms-like tyrosine kinase 3 receptor (Flt3) has an important role during early B-cell development, but the role of Flt3 in peripheral B cells has not been assessed before. Herein we describe a previously unappreciated role for Flt3 in IgG1 class-switch recombination (CSR) and production. We show that Flt3 is reexpressed on B-cell lymphoma 6(+) germinal center B cells in vivo and following LPS activation of peripheral B cells in vitro. Absence of Flt3 signaling in Flt3 ligand-deficient mice results in impaired IgG1 CSR and accumulation of IgM-secreting plasma cells. On activated B cells, Flt3 is coexpressed and functions in synergy with the common-gamma chain receptor family. B cells from Flt3 ligand-deficient mice have impaired IL-4R signaling, with reduced phosphorylation of signal transducer and activator of transcription (Stat) 6, and demonstrate a failure to initiate CSR to IgG1 with low expression of γ1 germ-line transcripts, resulting in impaired IgG1 production. Thus, functional synergy between Flt3 and IL-4R signaling is critical for Stat-mediated regulation of sterile γ1 germ-line transcripts and CSR to IgG1.

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