scholarly journals Simultaneous Presence of Non- and Highly Mutated Keyhole Limpet Hemocyanin (KLH)-Specific Plasmablasts Early after Primary KLH Immunization Suggests Cross-Reactive Memory B Cell Activation

2018 ◽  
Vol 200 (12) ◽  
pp. 3981-3992 ◽  
Author(s):  
Claudia Giesecke ◽  
Tim Meyer ◽  
Pawel Durek ◽  
Jochen Maul ◽  
Jan Preiß ◽  
...  
2018 ◽  
pp. 135
Author(s):  
Thomas L. Feldbush ◽  
Laura L. Stunz ◽  
David E. Lafrenz

2019 ◽  
Vol 31 (12) ◽  
pp. 771-779 ◽  
Author(s):  
Sarah Leach ◽  
Ryo Shinnakasu ◽  
Yu Adachi ◽  
Masatoshi Momota ◽  
Chieko Makino-Okamura ◽  
...  

Memory B cells protect against heterologous influenza infection


Rheumatology ◽  
2016 ◽  
Vol 56 (1) ◽  
pp. 134-144 ◽  
Author(s):  
Tim B. van der Houwen ◽  
P. Martin van Hagen ◽  
Wilhemina M. C. Timmermans ◽  
Sophinus J. W. Bartol ◽  
King H. Lam ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Emmanuelle Dugas-Bourdages ◽  
Sonia Néron ◽  
Annie Roy ◽  
André Darveau ◽  
Robert Delage

Persistent polyclonal B cell lymphocytosis (PPBL) is a rare disorder, diagnosed primarily in adult female smokers and characterized by an expansion of CD19+CD27+IgM+memory B cells, by the presence of binucleated lymphocytes, and by a moderate elevation of serum IgM. The clinical course is usually benign, but it is not known whether or not PPBL might be part of a process leading to the emergence of a malignant proliferative disorder. In this study we sought to investigate the functional response of B cells from patients with PPBL by use of an optimal memory B cell culture model based on the CD40-CD154 interaction. We found that the proliferation of PPBL B cells was almost as important as that of B cells from normal controls, resulting in high immunoglobulin secretion within vitroisotypic switching. We conclude that the CD40-CD154 activation pathway is functional in the memory B cell population of PPBL patients, suggesting that the disorder may be due to either a dysfunction of other cells in the microenvironment or a possible defect in another B cell activation pathway.


2015 ◽  
Vol 195 (12) ◽  
pp. 5592-5601 ◽  
Author(s):  
Sofia Järnum ◽  
Robert Bockermann ◽  
Anna Runström ◽  
Lena Winstedt ◽  
Christian Kjellman

2019 ◽  
Author(s):  
Felix Horns ◽  
Cornelia L. Dekker ◽  
Stephen R. Quake

AbstractAntibody memory protects humans from many diseases. Protective antibody memory responses require activation of transcriptional programs, cell proliferation, and production of antigen-specific antibodies, but how these aspects of the response are coordinated is poorly understood. We profiled the molecular and cellular features of the antibody response to influenza vaccination by integrating single-cell transcriptomics, longitudinal antibody repertoire sequencing, and antibody binding measurements. Single-cell transcriptional profiling revealed a program of memory B cell activation characterized by CD11c and T-bet expression associated with clonal expansion and differentiation toward effector function. Vaccination elicited an antibody clone which rapidly acquired broad high-affinity hemagglutinin binding during affinity maturation. Unexpectedly, many antibody clones elicited by vaccination do not bind vaccine, demonstrating non-specific activation of bystander antibodies by influenza vaccination. These results offer insight into how molecular recognition, transcriptional programs, and clonal proliferation are coordinated in the human B cell repertoire during memory recall.


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