scholarly journals Neutral maltase: the first human B-cell enzymatic marker reflecting terminal differentiation of mature B cells into plasma cells

Blood ◽  
1983 ◽  
Vol 62 (2) ◽  
pp. 505-508 ◽  
Author(s):  
PJ Philip ◽  
J Giudicelli ◽  
P Delque ◽  
JP Cassuto ◽  
P Sudaka ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Plasma Cells ◽  
Cell Lineage ◽  
Terminal Differentiation ◽  
Normal Subjects ◽  
Lymphoid Leukemia ◽  
Maltase Activity ◽  
Enzymatic Marker ◽  
B Lymphoid

Abstract Neutral maltase activity (alpha-D-glucoside glucohydrolase; EC: 3.2.1.20) was measured in B and T lymphocytes from peripheral blood of normal subjects and patients suffering from chronic or acute lymphoid leukemias. Neutral maltase activity is undetectable in T cells from normal subjects as well as in patients with chronic or acute T-lymphoid leukemias. Conversely, whereas this enzyme activity is always undetectable in chronic or acute B-lymphoid leukemia, neutral maltase activity is expressed in mature B cells from normal subjects. The detection of higher neutral maltase activity in plasma cells from myelomas than in normal B cells supports the concept that the expression of neutral maltase activity is related to the stages of differentiation and maturation reached by lymphocytes of the B-cell lineage. Neutral maltase therefore appears as the first B-cell enzymatic marker described that is expressed in the course of terminal differentiation of mature B cells into plasma cells.

scholarly journals Neutral maltase: the first human B-cell enzymatic marker reflecting terminal differentiation of mature B cells into plasma cells

Blood ◽  
1983 ◽  
Vol 62 (2) ◽  
pp. 505-508
Author(s):  
PJ Philip ◽  
J Giudicelli ◽  
P Delque ◽  
JP Cassuto ◽  
P Sudaka ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Plasma Cells ◽  
Cell Lineage ◽  
Terminal Differentiation ◽  
Normal Subjects ◽  
Lymphoid Leukemia ◽  
Maltase Activity ◽  
Enzymatic Marker ◽  
B Lymphoid

Neutral maltase activity (alpha-D-glucoside glucohydrolase; EC: 3.2.1.20) was measured in B and T lymphocytes from peripheral blood of normal subjects and patients suffering from chronic or acute lymphoid leukemias. Neutral maltase activity is undetectable in T cells from normal subjects as well as in patients with chronic or acute T-lymphoid leukemias. Conversely, whereas this enzyme activity is always undetectable in chronic or acute B-lymphoid leukemia, neutral maltase activity is expressed in mature B cells from normal subjects. The detection of higher neutral maltase activity in plasma cells from myelomas than in normal B cells supports the concept that the expression of neutral maltase activity is related to the stages of differentiation and maturation reached by lymphocytes of the B-cell lineage. Neutral maltase therefore appears as the first B-cell enzymatic marker described that is expressed in the course of terminal differentiation of mature B cells into plasma cells.

scholarly journals Interleukins and IgA synthesis. Human and murine interleukin 6 induce high rate IgA secretion in IgA-committed B cells.

1989 ◽  
Vol 169 (6) ◽  
pp. 2133-2148 ◽  
Author(s):  
K W Beagley ◽  
J H Eldridge ◽  
F Lee ◽  
H Kiyono ◽  
M P Everson ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Sharp Increase ◽  
Plasma Cells ◽  
Terminal Differentiation ◽  
Fold Increase ◽  
High Rate ◽  
Tnf Alpha ◽  
Ifn Gamma ◽  
Ig Synthesis

Freshly isolated murine PP B cells were cultured with 10 different cytokines, including IL-1 alpha, IL-2, IL-4, IL-5, IL-6, IL-7, IFN-gamma, TNF-alpha, and TGF-beta, to investigate a possible role for these cytokines in induction of Ig synthesis. Of interest was the finding that only IL-5 and both mouse recombinant (mr) and human recombinant (hr) IL-6 enhanced IgA synthesis. The effect was greater with either mrIL-6 or hrIL-6 than with mrIL-5. IL-6 induced cycling mIgA+ PP B cells to secrete high levels of IgA (approximately 7-fold increase over control). Of importance was the finding that mrIL-6 had little effect on secretion of IgM or IgG by PP B cell cultures. hrIL-6 also increased IgA secretion by PP B cells and this enhancement was abolished by a goat anti-hrIL-6 antiserum. mrIL-6 did not cause B cell proliferation but induced a sharp increase in numbers of B cells secreting IgA. Isotype-switching was not a mechanism for this marked increase in IgA synthesis since mIgA- PP B cells were not induced to secrete IgA by mrIL-6. From these studies we conclude that IL-6 plays an important role in promoting the terminal differentiation of PP B cells to IgA-secreting plasma cells.

scholarly journals The RNase III enzyme Dicer is essential for germinal center B-cell formation

Blood ◽  
2012 ◽  
Vol 119 (3) ◽  
pp. 767-776 ◽  
Author(s):  
Shengli Xu ◽  
Ke Guo ◽  
Qi Zeng ◽  
Jianxin Huo ◽  
Kong-Peng Lam
Keyword(s):  
B Cells ◽  
B Cell ◽  
Germinal Center ◽  
Plasma Cells ◽  
Cytidine Deaminase ◽  
Cell Formation ◽  
Terminal Differentiation ◽  
Mature Mirnas ◽  
Rnase Iii ◽  
Proapoptotic Protein

Abstract MicroRNAs (miRNAs) are short noncoding RNAs that regulate gene expression and are important for pre-B and follicular B lymphopoiesis as demonstrated, respectively, by mb-1-Cre– and cd19-Cre–mediated deletion of Dicer, the RNase III enzyme critical for generating mature miRNAs. To explore the role of miRNAs in B-cell terminal differentiation, we use Aicda-Cre to specifically delete Dicer in activated B cells where activation-induced cytidine deaminase is highly expressed. We demonstrate that mutant mice fail to produce high-affinity class-switched antibodies and generate memory B and long-lived plasma cells on immunization with a T cell–dependent antigen. More importantly, germinal center (GC) B-cell formation is drastically compromised in the absence of Dicer, as a result of defects in cell proliferation and survival. Dicer-deficient GC B cells express higher levels of cell cycle inhibitor genes and proapoptotic protein Bim. Ablation of Bim could partially rescue the defect in GC B-cell formation in Dicer-deficient mice. Taken together, our data suggest that Dicer and probably miRNAs are critical for GC B-cell formation during B-cell terminal differentiation.

scholarly journals The BTB-ZF transcription factor Zbtb20 is driven by Irf4 to promote plasma cell differentiation and longevity

2014 ◽  
Vol 211 (5) ◽  
pp. 827-840 ◽  
Author(s):  
Stéphane Chevrier ◽  
Dianne Emslie ◽  
Wei Shi ◽  
Tobias Kratina ◽  
Cameron Wellard ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
B Cells ◽  
B Cell ◽  
Plasma Cell ◽  
Cell Cycle Progression ◽  
Plasma Cells ◽  
Cell Lineage ◽  
B Cell Differentiation ◽  
Antibody Secreting Cell ◽  
Important Player

The transcriptional network regulating antibody-secreting cell (ASC) differentiation has been extensively studied, but our current understanding is limited. The mechanisms of action of known “master” regulators are still unclear, while the participation of new factors is being revealed. Here, we identify Zbtb20, a Bcl6 homologue, as a novel regulator of late B cell development. Within the B cell lineage, Zbtb20 is specifically expressed in B1 and germinal center B cells and peaks in long-lived bone marrow (BM) ASCs. Unlike Bcl6, an inhibitor of ASC differentiation, ectopic Zbtb20 expression in primary B cells facilitates terminal B cell differentiation to ASCs. In plasma cell lines, Zbtb20 induces cell survival and blocks cell cycle progression. Immunized Zbtb20-deficient mice exhibit curtailed humoral responses and accelerated loss of antigen-specific plasma cells, specifically from the BM pool. Strikingly, Zbtb20 induction does not require Blimp1 but depends directly on Irf4, acting at a newly identified Zbtb20 promoter in ASCs. These results identify Zbtb20 as an important player in late B cell differentiation and provide new insights into this complex process.

scholarly journals A monoclonal antibody that recognizes B cells and B cell precursors in mice.

1981 ◽  
Vol 153 (2) ◽  
pp. 269-279 ◽  
Author(s):  
R L Coffman ◽  
I L Weissman
Keyword(s):  
Monoclonal Antibody ◽  
Bone Marrow ◽  
B Cells ◽  
B Cell ◽  
Plasma Cells ◽  
Bone Marrow Cells ◽  
Cell Lineage ◽  
Hematopoietic Stem ◽  
B Cell Precursors

The monoclonal antibody, RA3-2C2, appears to be specific for cells within the B cell lineage. This antibody does not recognize thymocytes, peripheral T cells, or nonlymphoid hematopoietic cells in the spleen or bone marrow. Nor does it recognize the pluripotent hematopoietic stem cells, the spleen colony-forming unit, All sIg+ B cells and most plasma cells are RA3-2C2+. In addition, approximately 20% of nucleated bone marrow cells are RA3-2C2+ but sIg-. This population contains B cell precursors that can give rise to sIg+ cells within 2 d in vitro.

scholarly journals Occurrence of cytochrome b558 in B-cell lineage of human lymphocytes

Blood ◽  
1990 ◽  
Vol 75 (2) ◽  
pp. 458-461
Author(s):  
S Kobayashi ◽  
S Imajoh-Ohmi ◽  
M Nakamura ◽  
S Kanegasaki
Keyword(s):  
B Cells ◽  
Cell Surface ◽  
B Cell ◽  
B Lymphocytes ◽  
Plasma Cells ◽  
Human Lymphocytes ◽  
Cell Lineage ◽  
Superoxide Generation ◽  
Cell Stage ◽  
Cytochrome B558

Cytochrome b558, involved in superoxide generation in phagocytes, was found to be expressed on the cell surface of most normal peripheral B lymphocytes. The cytochrome was not found on the surface of peripheral T lymphocytes, natural killer cells, or peripheral lymphocytes derived from patients with X-linked chronic granulomatous disease. On stimulation, at least half of peripheral B lymphocytes could generate superoxide anion as detected by superoxide dismutase-sensitive nitroblue tetrazorium reduction. Cytochrome b558 was not present on the surface of pre-pre B cells or pre-B cells, but did appear at the early B-cell stage. It disappeared from the B-cell surface during terminal differentiation to plasma cells. The transient expression of the cytochrome in B-cell lineage may indicate that superoxide generation is important for the function of these cells at certain stages.

scholarly journals The transcription factors IRF8 and PU.1 negatively regulate plasma cell differentiation

2014 ◽  
Vol 211 (11) ◽  
pp. 2169-2181 ◽  
Author(s):  
Sebastian Carotta ◽  
Simon N. Willis ◽  
Jhagvaral Hasbold ◽  
Michael Inouye ◽  
Swee Heng Milon Pang ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Cell Differentiation ◽  
B Cells ◽  
B Cell ◽  
Plasma Cell ◽  
Plasma Cells ◽  
Terminal Differentiation ◽  
Plasma Cell Differentiation ◽  
Class Switch ◽  
Complex Functions

Activated B cells undergo immunoglobulin class-switch recombination (CSR) and differentiate into antibody-secreting plasma cells. The distinct transcriptomes of B cells and plasma cells are maintained by the antagonistic influences of two groups of transcription factors: those that maintain the B cell program, including BCL6 and PAX5, and plasma cell–promoting factors, such as IRF4 and BLIMP-1. We show that the complex of IRF8 and PU.1 controls the propensity of B cells to undergo CSR and plasma cell differentiation by concurrently promoting the expression of BCL6 and PAX5 and repressing AID and BLIMP-1. As the PU.1–IRF8 complex functions in a reciprocal manner to IRF4, we propose that concentration-dependent competition between these factors controls B cell terminal differentiation.

scholarly journals Suppression of Signal Transducer and Activator of Transcription 3–Dependent B Lymphocyte Terminal Differentiation by Bcl-6

2000 ◽  
Vol 192 (12) ◽  
pp. 1841-1848 ◽  
Author(s):  
Rajko Reljic ◽  
Simon D. Wagner ◽  
Luke J. Peakman ◽  
Douglas T. Fearon
Keyword(s):  
B Cells ◽  
B Cell ◽  
B Lymphocyte ◽  
Plasma Cells ◽  
Somatic Hypermutation ◽  
Terminal Differentiation ◽  
Cell Development ◽  
Signal Transducer ◽  
Effector Cells ◽  
Transcription 3

Lymphocytes usually differentiate into effector cells within days after antigen exposure, except in germinal centers where terminal differentiation is delayed while somatic hypermutation creates high-affinity antibody mutants. Here we investigate whether arrest of terminal differentiation can be mediated by BCL-6, a transcriptional repressor that is expressed by germinal center B cells and is required for this phase of B cell development. We find that BCL-6 suppresses the differentiation of transformed and primary B cells to plasma cells by inhibiting the signal transducer and activator of transcription 3–dependent expression of the major regulator of plasma cell development, the B lymphocyte–induced maturation protein (Blimp-1). This function of BCL-6 as a repressor of B lymphocyte differentiation may also underlie the association between chromosomal translocations of its gene and B cell lymphomas.

scholarly journals Memory B Cells Are Biased Towards Terminal Differentiation: A Strategy That May Prevent Repertoire Freezing

1997 ◽  
Vol 186 (6) ◽  
pp. 931-940 ◽  
Author(s):  
Christophe Arpin ◽  
Jacques Banchereau ◽  
Yong-Jun Liu
Keyword(s):  
Cell Differentiation ◽  
B Cells ◽  
B Cell ◽  
Plasma Cell ◽  
Plasma Cells ◽  
Cell Clone ◽  
Terminal Differentiation ◽  
Memory B Cells ◽  
B Cell Differentiation

Isolation of large numbers of surface IgD+CD38− naive and surface IgD−CD38− memory B cells allowed us to study the intrinsic differences between these two populations. Upon in vitro culture with IL-2 and IL-10, human CD40–activated memory B cells undergo terminal differentiation into plasma cells more readily than do naive B cells, as they give rise to five- to eightfold more plasma cells and three- to fourfold more secreted immunoglobulins. By contrast, naive B cells give rise to a larger number of nondifferentiated B blasts. Saturating concentrations of CD40 ligand, which fully inhibit naive B cell differentiation, only partially affect that of memory B cells. The propensity of memory B cells to undergo terminal plasma cell differentiation may explain the extensive extra follicular plasma cell reaction and the limited germinal center reaction observed in vivo after secondary immunizations, which contrast with primary responses in carrier-primed animals. This unique feature of memory B cells may confer two important capacities to the immune system: (a) the rapid generation of a large number of effector cells to efficiently eliminate the pathogens; and (b) the prevention of the overexpansion and chronic accumulation of one particular memory B cell clone that would freeze the available peripheral repertoire.

scholarly journals Occurrence of cytochrome b558 in B-cell lineage of human lymphocytes

Blood ◽  
1990 ◽  
Vol 75 (2) ◽  
pp. 458-461 ◽  
Author(s):  
S Kobayashi ◽  
S Imajoh-Ohmi ◽  
M Nakamura ◽  
S Kanegasaki
Keyword(s):  
B Cells ◽  
Cell Surface ◽  
B Cell ◽  
B Lymphocytes ◽  
Plasma Cells ◽  
Human Lymphocytes ◽  
Cell Lineage ◽  
Superoxide Generation ◽  
Cell Stage ◽  
Cytochrome B558

Abstract Cytochrome b558, involved in superoxide generation in phagocytes, was found to be expressed on the cell surface of most normal peripheral B lymphocytes. The cytochrome was not found on the surface of peripheral T lymphocytes, natural killer cells, or peripheral lymphocytes derived from patients with X-linked chronic granulomatous disease. On stimulation, at least half of peripheral B lymphocytes could generate superoxide anion as detected by superoxide dismutase-sensitive nitroblue tetrazorium reduction. Cytochrome b558 was not present on the surface of pre-pre B cells or pre-B cells, but did appear at the early B-cell stage. It disappeared from the B-cell surface during terminal differentiation to plasma cells. The transient expression of the cytochrome in B-cell lineage may indicate that superoxide generation is important for the function of these cells at certain stages.

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