Peripheral B cell receptor editing may promote the production of high-affinity autoantibodies in CD22-deficient mice

2006 ◽  
Vol 36 (10) ◽  
pp. 2755-2767 ◽  
Author(s):  
Yuval Yarkoni ◽  
Ruth Fischel ◽  
Inbal Kat ◽  
Nurit Yachimovich-Cohen ◽  
Dan Eilat
Keyword(s):  
B Cell ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Receptor Editing ◽  
High Affinity ◽  
Deficient Mice

scholarly journals Autoimmune NZB/NZW F1 mice utilize B cell receptor editing for generating high-affinity anti-dsDNA autoantibodies from low-affinity precursors

2003 ◽  
Vol 33 (9) ◽  
pp. 2469-2478 ◽  
Author(s):  
Nurit Yachimovich-Cohen ◽  
Ruth Fischel ◽  
Neta Bachar ◽  
Yuval Yarkoni ◽  
Dan Eilat
Keyword(s):  
B Cell ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Receptor Editing ◽  
High Affinity

B cell receptor editing in tolerance and autoimmunity

10.2741/2217 ◽  
2007 ◽  
Vol 12 (1) ◽  
pp. 2136 ◽  
Author(s):  
Hilla Azulay-Debby
Keyword(s):  
B Cell ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Receptor Editing

scholarly journals Discovery of high affinity anti-ricin antibodies by B cell receptor sequencing and by yeast display of combinatorial VH:VLlibraries from immunized animals

mAbs ◽  
2016 ◽  
Vol 8 (6) ◽  
pp. 1035-1044 ◽  
Author(s):  
Bo Wang ◽  
Chang-Han Lee ◽  
Erik L. Johnson ◽  
Christien A. Kluwe ◽  
Josephine C. Cunningham ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Yeast Display ◽  
High Affinity

Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling

2005 ◽  
Vol 7 (2) ◽  
pp. 199-206 ◽  
Author(s):  
Brian E Collins ◽  
Brian A Smith ◽  
Per Bengtson ◽  
James C Paulson
Keyword(s):  
B Cell ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Receptor Signaling ◽  
B Cell Receptor Signaling ◽  
Deficient Mice ◽  
Cell Receptor Signaling

scholarly journals BCR Affinity Influences T-B Interactions and B Cell Development in Secondary Lymphoid Organs

2021 ◽  
Vol 12 ◽  
Author(s):  
Alec J. Wishnie ◽  
Tzippora Chwat-Edelstein ◽  
Mary Attaway ◽  
Bao Q. Vuong
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cell Receptor ◽  
Cell Development ◽  
B Cell Development ◽  
Affinity Maturation ◽  
B Cell Receptor ◽  
Specific Cell ◽  
High Affinity ◽  
Tfh Cells

B cells produce high-affinity immunoglobulins (Igs), or antibodies, to eliminate foreign pathogens. Mature, naïve B cells expressing an antigen-specific cell surface Ig, or B cell receptor (BCR), are directed toward either an extrafollicular (EF) or germinal center (GC) response upon antigen binding. B cell interactions with CD4+ pre-T follicular helper (pre-Tfh) cells at the T-B border and effector Tfh cells in the B cell follicle and GC control B cell development in response to antigen. Here, we review recent studies demonstrating the role of B cell receptor (BCR) affinity in modulating T-B interactions and the subsequent differentiation of B cells in the EF and GC response. Overall, these studies demonstrate that B cells expressing high affinity BCRs preferentially differentiate into antibody secreting cells (ASCs) while those expressing low affinity BCRs undergo further affinity maturation or differentiate into memory B cells (MBCs).

scholarly journals The distinctive germinal center phase of IgE+ B lymphocytes limits their contribution to the classical memory response

2013 ◽  
Vol 210 (12) ◽  
pp. 2755-2771 ◽  
Author(s):  
Jin-Shu He ◽  
Michael Meyer-Hermann ◽  
Deng Xiangying ◽  
Lim Yok Zuan ◽  
Leigh Ann Jones ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
B Cell ◽  
Germinal Center ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Comprehensive Model ◽  
B Cell Differentiation ◽  
Memory Response ◽  
High Affinity ◽  
Sequential Switching

The mechanisms involved in the maintenance of memory IgE responses are poorly understood, and the role played by germinal center (GC) IgE+ cells in memory responses is particularly unclear. IgE+ B cell differentiation is characterized by a transient GC phase, a bias toward the plasma cell (PC) fate, and dependence on sequential switching for the production of high-affinity IgE. We show here that IgE+ GC B cells are unfit to undergo the conventional GC differentiation program due to impaired B cell receptor function and increased apoptosis. IgE+ GC cells fail to populate the GC light zone and are unable to contribute to the memory and long-lived PC compartments. Furthermore, we demonstrate that direct and sequential switching are linked to distinct B cell differentiation fates: direct switching generates IgE+ GC cells, whereas sequential switching gives rise to IgE+ PCs. We propose a comprehensive model for the generation and memory of IgE responses.

scholarly journals Partial block in B lymphocyte development at the transition into the pre-B cell receptor stage in Vpre-B1-deficient mice

1999 ◽  
Vol 11 (3) ◽  
pp. 453-460 ◽  
Author(s):  
Annica Mårtensson ◽  
Yair Argon ◽  
Fritz Melchers ◽  
Jeanne L. Duland ◽  
Inga-Lill Mårtensson
Keyword(s):  
B Cell ◽  
B Lymphocyte ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Lymphocyte Development ◽  
B Lymphocyte Development ◽  
Deficient Mice
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