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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Bemark, Mats Jonsson, Ing-marie Bokarewa, Maria I. Andersson, Karin M. E. Erlandsson, Malin C. Nurkkala-karlsson, Merja Brisslert, Mikael Wasén, Caroline Svensson, Mattias N. D. |
| Description | Author Affiliation: Svensson MN ( Department of Rheumatology and Inflammation Research at Sahlgrenska Academy, University of Gothenburg, Gothenburg 41346, Sweden); Andersson KM ( Department of Rheumatology and Inflammation Research at Sahlgrenska Academy, University of Gothenburg, Gothenburg 41346, Sweden); Wasén C ( Department of Rheumatology and Inflammation Research at Sahlgrenska Academy, University of Gothenburg, Gothenburg 41346, Sweden); Erlandsson MC ( Department of Rheumatology and Inflammation Research at Sahlgrenska Academy, University of Gothenburg, Gothenburg 41346, Sweden); Nurkkala-Karlsson M ( Department of Rheumatology and Inflammation Research at Sahlgrenska Academy, University of Gothenburg, Gothenburg 41346, Sweden); Jonsson IM ( Department of Rheumatology and Inflammation Research at Sahlgrenska Academy, University of Gothenburg, Gothenburg 41346, Sweden); Brisslert M ( Department of Rheumatology and Inflammation Research at Sahlgrenska Academy, University of Gothenburg, Gothenburg 41346, Sweden); Bemark M ( Department of Microbiology and Immunology at Sahlgrenska Academy, University of Gothenburg, Gothenburg 41390, Sweden.); Bokarewa MI ( Department of Rheumatology and Inflammation Research at Sahlgrenska Academy, University of Gothenburg, Gothenburg 41346, Sweden); |
| 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. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 48 |
| Volume Number | 112 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2015-12-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | B-Lymphocytes Immunology Germinal Center Immunoglobulin Class Switching Immunoglobulin G Fms-Like Tyrosine Kinase 3 Physiology Animals Apoptosis Gene Expression Regulation Immunoglobulin M Ligands Lymphocyte Activation Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Plasma Cells Receptors, Interleukin-4 Metabolism Signal Transduction Genetics Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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