Artikel ; Online: BAFFR controls early memory B cell responses but is dispensable for germinal center function.
The Journal of experimental medicine
2020 Band 218, Heft 2
Abstract: The TNF superfamily ligand BAFF maintains the survival of naive B cells by signaling through its surface receptor, BAFFR. Activated B cells maintain expression of BAFFR after they differentiate into germinal center (GC) or memory B cells (MBCs). However, ...
Abstract | The TNF superfamily ligand BAFF maintains the survival of naive B cells by signaling through its surface receptor, BAFFR. Activated B cells maintain expression of BAFFR after they differentiate into germinal center (GC) or memory B cells (MBCs). However, the functions of BAFFR in these antigen-experienced B cell populations remain unclear. Here, we show that B cell-intrinsic BAFFR does not play a significant role in the survival or function of GC B cells or in the generation of the somatically mutated MBCs derived from them. Instead, BAFF/BAFFR signaling was required to generate the unmutated, GC-independent MBCs that differentiate directly from activated B cell blasts early in the response. Furthermore, amplification of BAFFR signaling in responding B cells did not affect GCs or the generation of GC-derived MBCs but greatly expanded the GC-independent MBC response. Although BAFF/BAFFR signaling specifically controlled the formation of the GC-independent MBC response, both types of MBCs required input from this pathway for optimal long-term survival. |
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Mesh-Begriff(e) | Animals ; B-Cell Activating Factor/immunology ; B-Cell Activating Factor/metabolism ; B-Cell Activation Factor Receptor/immunology ; B-Cell Activation Factor Receptor/metabolism ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Germinal Center/immunology ; Germinal Center/metabolism ; Immunologic Memory/immunology ; Mice ; Mice, Inbred C57BL ; Signal Transduction/physiology |
Chemische Substanzen | B-Cell Activating Factor ; B-Cell Activation Factor Receptor ; Tnfrsf13c protein, mouse |
Sprache | Englisch |
Erscheinungsdatum | 2020-11-23 |
Erscheinungsland | United States |
Dokumenttyp | Journal Article ; Research Support, Non-U.S. Gov't |
ZDB-ID | 218343-2 |
ISSN | 1540-9538 ; 0022-1007 |
ISSN (online) | 1540-9538 |
ISSN | 0022-1007 |
DOI | 10.1084/jem.20191167 |
Datenquelle | MEDical Literature Analysis and Retrieval System OnLINE |
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