scholarly journals VprBP Is Required for Efficient Editing and Selection of Igκ+ B Cells, but Is Dispensable for Igλ+ and Marginal Zone B Cell Maturation and Selection

2015 ◽  
Vol 195 (4) ◽  
pp. 1524-1537 ◽  
Author(s):  
Victoria L. Palmer ◽  
Razia Aziz-Seible ◽  
Michele D. Kassmeier ◽  
Mary Rothermund ◽  
Greg A. Perry ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Marginal Zone ◽  
Cell Maturation ◽  
B Cell Maturation ◽  
Selection Of

scholarly journals Characterization of marginal zone B cell precursors

2005 ◽  
Vol 202 (9) ◽  
pp. 1225-1234 ◽  
Author(s):  
Bhaskar Srivastava ◽  
William J. Quinn ◽  
Kristin Hazard ◽  
Jan Erikson ◽  
David Allman
Keyword(s):  
B Cells ◽  
B Cell ◽  
Marginal Zone ◽  
Environmental Cues ◽  
Developmental Potential ◽  
B Cell Maturation ◽  
B Cell Precursors ◽  
Follicular B Cells ◽  
Selection Of

Selection of recently formed B cells into the follicular or marginal zone (MZ) compartments is proposed to occur by way of proliferative intermediates expressing high levels of CD21/35 and CD23. However, we show that CD21/35high CD23+ splenocytes are not enriched for proliferative cells, and do not contribute substantially to the generation of follicular B cells. Instead, ontogenic relationships, steady-state labeling kinetics, and adoptive transfer experiments suggest that CD21/35high CD23+ splenocytes serve primarily as precursors for MZ B cells, although their developmental potential seems to be broader and is influenced by environmental cues that are associated with lymphopenia. Furthermore, CD21/35high CD23+ splenocytes share several key functional characteristics with MZ B cells, including their capacity to trap T-independent antigen and a heightened proliferative response to LPS. These observations challenge previous models of peripheral B cell maturation, and suggest that MZ B cells develop by way of CD21/35high CD23+ intermediates.

scholarly journals Maturation of Marginal Zone and Follicular B Cells Requires B Cell Activating Factor of the Tumor Necrosis Factor Family and Is Independent of B Cell Maturation Antigen

2001 ◽  
Vol 194 (11) ◽  
pp. 1691-1698 ◽  
Author(s):  
Pascal Schneider ◽  
Hisakazu Takatsuka ◽  
Anne Wilson ◽  
Fabienne Mackay ◽  
Aubry Tardivel ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Tumor Necrosis ◽  
Marginal Zone ◽  
Cell Maturation ◽  
Soluble Form ◽  
B Cell Maturation ◽  
B Cell Activating Factor ◽  
Necrosis Factor ◽  
B Cell Maturation Antigen

B cells undergo a complex series of maturation and selection steps in the bone marrow and spleen during differentiation into mature immune effector cells. The tumor necrosis factor (TNF) family member B cell activating factor of the TNF family (BAFF) (BLyS/TALL-1) plays an important role in B cell homeostasis. BAFF and its close homologue a proliferation-inducing ligand (APRIL) have both been shown to interact with at least two receptors, B cell maturation antigen (BCMA) and transmembrane activator and cyclophilin ligand interactor (TACI), however their relative contribution in transducing BAFF signals in vivo remains unclear. To functionally inactivate both BAFF and APRIL, mice transgenic for a soluble form of TACI were generated. They display a developmental block of B cell maturation in the periphery, leading to a severe depletion of marginal zone and follicular B2 B cells, but not of peritoneal B1 B cells. In contrast, mice transgenic for a soluble form of BCMA, which binds APRIL, have no detectable B cell phenotype. This demonstrates a crucial role for BAFF in B cell maturation and strongly suggests that it signals via a BCMA-independent pathway and in an APRIL-dispensable way.

scholarly journals Targeted selection of HIV-specific antibody mutations by engineering B cell maturation

Science ◽  
2019 ◽  
Vol 366 (6470) ◽  
pp. eaay7199 ◽  
Author(s):  
Kevin O. Saunders ◽  
Kevin Wiehe ◽  
Ming Tian ◽  
Priyamvada Acharya ◽  
Todd Bradley ◽  
...  
Keyword(s):  
B Cell ◽  
Specific Antibody ◽  
Cell Maturation ◽  
B Cell Maturation ◽  
Selection Of

Evidence for B cell maturation but not trained immunity in uninfected infants exposed to hepatitis C virus

Gut ◽  
2020 ◽  
Vol 69 (12) ◽  
pp. 2203-2213 ◽  
Author(s):  
Anton Lutckii ◽  
Benedikt Strunz ◽  
Anton Zhirkov ◽  
Olga Filipovich ◽  
Elena Rukoiatkina ◽  
...  
Keyword(s):  
Immune System ◽  
B Cells ◽  
B Cell ◽  
Immune Cells ◽  
Immune Cell ◽  
Innate Immune ◽  
Cell Maturation ◽  
Innate Immune Cells ◽  
B Cell Maturation ◽  
Exposed Uninfected

ObjectivesVertical transmission of hepatitis C virus (HCV) is rare compared with other chronic viral infections, despite that newborns have an immature, and possibly more susceptible, immune system. It further remains unclear to what extent prenatal and perinatal exposure to HCV affects immune system development in neonates.DesignTo address this, we studied B cells, innate immune cells and soluble factors in a cohort of 62 children that were either unexposed, exposed uninfected or infected with HCV. Forty of these infants were followed longitudinally from birth up until 18 months of age.ResultsAs expected, evidence for B cell maturation was observed with increased age in children, whereas few age-related changes were noticed among innate immune cells. HCV-infected children had a high frequency of HCV-specific IgG-secreting B cells. Such a response was also detected in some exposed but uninfected children but not in uninfected controls. Consistent with this, both HCV-exposed uninfected and HCV-infected infants had evidence of early B cell immune maturation with an increased proportion of IgA-positive plasma cells and upregulated CD40 expression. In contrast, actual HCV viraemia, but not mere exposure, led to alterations within myeloid immune cell populations, natural killer (NK) cells and a distinct soluble factor profile with increased levels of inflammatory cytokines and chemokines.ConclusionOur data reveal that exposure to, and infection with, HCV causes disparate effects on adaptive B cells and innate immune cell such as myeloid cells and NK cells in infants.

scholarly journals Baff Binds to the Tumor Necrosis Factor Receptor–Like Molecule B Cell Maturation Antigen and Is Important for Maintaining the Peripheral B Cell Population

2000 ◽  
Vol 192 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Jeffrey S. Thompson ◽  
Pascal Schneider ◽  
Susan L. Kalled ◽  
LiChun Wang ◽  
Eric A. Lefevre ◽  
...  
Keyword(s):  
B Cells ◽  
Tumor Necrosis Factor ◽  
B Cell ◽  
Cell Population ◽  
Tumor Necrosis ◽  
Cell Maturation ◽  
Soluble Form ◽  
B Cell Maturation ◽  
Necrosis Factor ◽  
B Cell Maturation Antigen

The tumor necrosis factor (TNF) family member B cell activating factor (BAFF) binds B cells and enhances B cell receptor–triggered proliferation. We find that B cell maturation antigen (BCMA), a predicted member of the TNF receptor family expressed primarily in mature B cells, is a receptor for BAFF. Although BCMA was previously localized to the Golgi apparatus, BCMA was found to be expressed on the surface of transfected cells and tonsillar B cells. A soluble form of BCMA, which inhibited the binding of BAFF to a B cell line, induced a dramatic decrease in the number of peripheral B cells when administered in vivo. Moreover, culturing splenic cells in the presence of BAFF increased survival of a percentage of the B cells. These results are consistent with a role for BAFF in maintaining homeostasis of the B cell population.

scholarly journals SHEP1 partners with CasL to promote marginal zone B-cell maturation

2010 ◽  
Vol 107 (44) ◽  
pp. 18944-18949 ◽  
Author(s):  
C. D. Browne ◽  
M. M. Hoefer ◽  
S. K. Chintalapati ◽  
M. H. Cato ◽  
Y. Wallez ◽  
...  
Keyword(s):  
B Cell ◽  
Marginal Zone ◽  
Cell Maturation ◽  
B Cell Maturation

Dμ expression causes enrichment of MZ B cells, but is non permissive for B cell maturation in Rag2−/− mice even if combined with Bcl-2

2006 ◽  
Vol 43 (9) ◽  
pp. 1316-1324 ◽  
Author(s):  
Ingela Wikström ◽  
Ingela Bergqvist ◽  
Dan Holmberg ◽  
Johan Forssell
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cell Maturation ◽  
B Cell Maturation

scholarly journals E3 Ligase UBR5 HECT domain mutations in lymphoma control maturation of B cells via alternative splicing

2019 ◽  
Author(s):  
Samantha A. Swenson ◽  
Tyler J. Gilbreath ◽  
Heather Vahle ◽  
R. Willow Hynes-Smith ◽  
Jared H. Graham ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
B Cells ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Development ◽  
Cell Maturation ◽  
Hect Domain ◽  
B Cell Maturation ◽  
Mantle Cell

ABSTRACTCoordination of a number of molecular mechanisms including transcription, alternative splicing, and class switch recombination are required to facilitate development, activation, and survival of B cells. Disruption of these pathways can result in malignant transformation. Recently, next generation sequencing has identified a number of novel mutations in mantle cell lymphoma (MCL) patients including the ubiquitin E3 ligase UBR5. Approximately 18% of MCL patients were found to have mutations in UBR5 with the majority of mutations within the HECT domain of the protein which can accept and transfer ubiquitin molecules to the substrate. Determining if UBR5 controls the maturation of B cells is important to fully understand malignant transformation to MCL. To elucidate the role of UBR5 in B cell maturation and activation we generated a conditional mutant disrupting UBR5’s C-terminal HECT domain. Loss of the UBR5 HECT domain leads to a block in maturation of B cells in the spleen and up-regulation of proteins associated with mRNA splicing via the spliceosome. Our studies reveal a novel role of UBR5 in B cell maturation by regulating alternative splicing of key transcripts during B cell development and suggests UBR5 mutations may promote mantle cell lymphoma initiation.KEY POINTSUtilizing a novel mouse model mimicking MCL patient mutations, the loss of UBR5’s HECT domain causes alterations in B cell development.UBR5 mutations lead to stabilization of UBR5 and aberrant splicing.

scholarly journals Intracellular BH3 profiling reveals shifts in anti-apoptotic dependency in B-cell maturation and activation

2017 ◽  
Author(s):  
Joanne Dai ◽  
Micah A. Luftig
Keyword(s):  
B Cells ◽  
B Cell ◽  
Plasma Cells ◽  
Human Peripheral Blood ◽  
Survival Strategies ◽  
Cell Maturation ◽  
Barr Virus ◽  
B Cell Maturation ◽  
Human B Cells ◽  
Activated B Cells

AbstractApoptosis is critical to B-cell maturation, but studies of apoptotic regulation in primary human B cells is lacking. Previously, we found that infecting human B cells with Epstein-Barr virus induces two different survival strategies (Priceet al., 2017). Here, we sought to better understand the mechanisms of apoptotic regulation in normal and activated B cells. Using intracellular BH3 profiling (iBH3), we defined the Bcl2-dependency of B-cell subsets from human peripheral blood and tonsillar lymphoid tissue as well as mitogen-activated B cells. We found that naïve and memory B cells were BCL-2 dependent, while germinal center B cells were MCL-1 dependent and plasma cells were BCL-XL dependent. Proliferating B cells activated by CpG or CD40L/IL-4 became more dependent upon MCL-1 and BCL-XL. As B-cell lymphomas often rely on survival mechanisms derived from normal and activated B cells, these findings offer new insight into potential therapeutic strategies for lymphomas.

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