Primary in vitro antibody response of rabbit lymphoid cells and T-B cell collaboration in the absence of detectable mitogens

1977 ◽  
Vol 32 (1) ◽  
pp. 23-35 ◽  
Author(s):  
Dennis W. Metzger ◽  
Robert L. Hendricks ◽  
Marius Teodorescu ◽  
Sheldon Dray
Keyword(s):  
Antibody Response ◽  
B Cell ◽  
Lymphoid Cells

scholarly journals Monoclonal antibodies to the 140,000 mol wt glycoprotein of B lymphocyte membranes (CR2 receptor) initiates proliferation of B cells in vitro

Blood ◽  
1985 ◽  
Vol 66 (4) ◽  
pp. 824-829
Author(s):  
BS Wilson ◽  
JL Platt ◽  
NE Kay
Keyword(s):  
Monoclonal Antibodies ◽  
B Cells ◽  
B Cell ◽  
Peripheral Blood ◽  
B Lymphocyte ◽  
Human Peripheral Blood ◽  
Raji Cell ◽  
Lymphoid Cells ◽  
Humoral Immune

Several mouse monoclonal IgG antibodies (AB1, AB2, AB3, and AB5) were developed that reacted with a 140,000 mol wt glycoprotein on the surface of cultured RAJI B lymphoid cells. The antibodies reacted with purified normal human peripheral blood B cells and CLL Ig+ B cells and showed specific germinal center and mantle zone staining in tissue sections of secondary lymphoid organs. Immunodepletion studies using 125I surface-labeled Raji cell membrane antigens demonstrated that the antigen identified by AB5 is the same 140,000 mol wt glycoprotein detected by anti-B2 that has recently been shown to react with the C3d fragment or CR2 receptor. (Iida et al: J Exp Med 158:1021, 1983). Addition of the AB series and anti-B2 monoclonal antibodies to cultures of purified human peripheral blood B cells resulted in the uptake of 3H- thymidine at two to six times background control levels provided that irradiated autologous T cells were added to the culture. Stimulation was not evoked by other monoclonal antibodies to B cell surface molecules (ie, B1, BA-1, BA-2, and HLA-DR). Pepsin-generated F(ab')2 fragments of anti-CR2 antibodies were essentially as effective as the intact IgG molecule in stimulating B cells. Induction of B cell proliferation by antibody binding to CR2 suggests that the C3d receptor may have an integral role in regulation of humoral immune response.

scholarly journals Terminal Deoxynucleotidyl Transferase Is Not Required for Antibody Response to Polysaccharide Vaccines againstStreptococcus pneumoniaeandSalmonella entericaSerovar Typhi

2018 ◽  
Vol 86 (9) ◽  
Author(s):  
Vivek Belde ◽  
Matthew P. Cravens ◽  
Dania Gulandijany ◽  
Justin A. Walker ◽  
Isabel Palomo-Caturla ◽  
...  
Keyword(s):  
Antibody Response ◽  
B Cell ◽  
Salmonella Enterica ◽  
Passive Immunization ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Human Infants ◽  
Content Type ◽  
Serovar Typhimurium

ABSTRACTB cell antigen receptor (BCR) diversity increases by several orders of magnitude due to the action of terminal deoxynucleotidyl transferase (TdT) during V(D)J recombination. Unlike adults, infants have limited BCR diversity, in part due to reduced expression of TdT. Since human infants and young mice respond poorly to polysaccharide vaccines, such as the pneumococcal polysaccharide vaccine Pneumovax23 and Vi polysaccharide (ViPS) ofSalmonella entericaserovar Typhi, we tested the contribution of TdT-mediated BCR diversity in response to these vaccines. We found that TdT+/−and TdT−/−mice generated comparable antibody responses to Pneumovax23 and survivedStreptococcus pneumoniaechallenge. Moreover, passive immunization of B cell-deficient mice with serum from Pneumovax23-immunized TdT+/−or TdT−/−mice conferred protection. TdT+/−and TdT−/−mice generated comparable levels of anti-ViPS antibodies and antibody-dependent, complement-mediated bactericidal activity againstS. Typhiin vitro. To test the protective immunity conferred by ViPS immunizationin vivo, TdT+/−and TdT−/−mice were challenged with a chimericSalmonella entericaserovar Typhimurium strain expressing ViPS, since mice are nonpermissive hosts forS. Typhi infection. Compared to their unimmunized counterparts, immunized TdT+/−and TdT−/−mice challenged with ViPS-expressingS. Typhimurium exhibited a significant reduction in the bacterial burden and liver pathology. These data suggest that the impaired antibody response to the Pneumovax23 and ViPS vaccines in the young is not due to limited TdT-mediated BCR diversification.

scholarly journals Specific adsorption of IgM antibody onto H-2-activated mouse T lymphocytes.

1976 ◽  
Vol 143 (2) ◽  
pp. 444-449 ◽  
Author(s):  
L Hudson ◽  
J Sprent
Keyword(s):  
T Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Progenitor Cell ◽  
Lymphoid Cells ◽  
Immunofluorescent Staining ◽  
Cell Populations ◽  
Activated T Cells ◽  
Specific Manner

Evidence is presented to support the contention that IgM demonstrable by surface immunofluorescent staining on H-2-activated T cells represents specifically adsorbed B-cell-derived alloantibody. T cells activated to H-2 determinants expressed surface IgM only when the progenitor cell populations contained B lymphocytes. IgM was not detected on T cells activated to determinants which fail to stimulate alloantibody production (e.g., M-locus determinants). In addition, IgM-negative H-2 activated T cells (derived from B-cell-depleted lymphoid cells), unlike M-locus-activated T cells, adsorbed IgM in a specific manner when incubated in vitro with "early bleed" antisera raised against the activating H-2 determinants.

scholarly journals Clarifying the role of Stat5 in lymphoid development and Abelson-induced transformation

Blood ◽  
2006 ◽  
Vol 107 (12) ◽  
pp. 4898-4906 ◽  
Author(s):  
Andrea Hoelbl ◽  
Boris Kovacic ◽  
Marc A. Kerenyi ◽  
Olivia Simma ◽  
Wolfgang Warsch ◽  
...  
Keyword(s):  
B Cell ◽  
Fetal Liver ◽  
Transgenic Animals ◽  
Cell Receptor ◽  
Lymphoid Cells ◽  
In Vitro Assays ◽  
Cell Stage ◽  
Lymphoid Development ◽  
B Lymphoid

AbstractThe Stat5 transcription factors Stat5a and Stat5b have been implicated in lymphoid development and transformation. Most studies have employed Stat5a/b-deficient mice where gene targeting disrupted the first protein-coding exon, resulting in the expression of N-terminally truncated forms of Stat5a/b (Stat5a/bΔN/ΔN mice). We have now reanalyzed lymphoid development in Stat5a/bnull/null mice having a complete deletion of the Stat5a/b gene locus. The few surviving Stat5a/bnull/null mice lacked CD8+ T lymphocytes. A massive reduction of CD8+ T cells was also found in Stat5a/bfl/fllck-cre transgenic animals. While γδ T-cell receptor–positive (γδTCR+) cells were expressed at normal levels in Stat5a/bΔN/ΔN mice, they were completely absent in Stat5a/bnull/null animals. Moreover, B-cell maturation was abrogated at the pre–pro-B-cell stage in Stat5a/bnull/null mice, whereas Stat5a/bΔN/ΔN B-lymphoid cells developed to the early pro-B-cell stage. In vitro assays using fetal liver-cell cultures confirmed this observation. Most strikingly, Stat5a/bnull/null cells were resistant to transformation and leukemia development induced by Abelson oncogenes, whereas Stat5a/bΔN/ΔN-derived cells readily transformed. These findings show distinct lymphoid defects for Stat5a/bΔN/ΔN and Stat5a/bnull/null mice and define a novel functional role for the N-termini of Stat5a/b in B-lymphoid transformation.

scholarly journals DIRECT AND INDIRECT EFFECTS OF X-RADIATION ON ANTIBODY-PRODUCING CELLS

1957 ◽  
Vol 105 (5) ◽  
pp. 417-424 ◽  
Author(s):  
Frank J. Dixon ◽  
James C. Roberts ◽  
William O. Weigle
Keyword(s):  
Antibody Response ◽  
Indirect Effects ◽  
Lymphoid Tissue ◽  
Radiation Injury ◽  
Inhibitory Effect ◽  
Significant Inhibition ◽  
Lymphoid Cells ◽  
Whole Body ◽  
Direct And Indirect Effects

X-radiation appears to exert its inhibitory effect on the antibody response by two mutually dependent routes: (a) direct radiation injury to the antibody-producing lymphoid tissue, and (b) indirect effects of altered homeostasis in the radiated host on antibody-producing tissues. Neither of these two effects alone produces significant inhibition of the secondary antibody response made by transferred lymphoid cells. However, 400 to 500 r administered in vitro to the transferred cells, plus 400 r whole body x-radiation of the recipient prior to transfer, completely inhibited the antibody response.

scholarly journals Expression of interleukin-4 receptors on early human B-lineage cells

Blood ◽  
1991 ◽  
Vol 78 (3) ◽  
pp. 703-710 ◽  
Author(s):  
CL Law ◽  
RJ Armitage ◽  
JG Villablanca ◽  
TW LeBien
Keyword(s):  
Bone Marrow ◽  
B Cell ◽  
Constitutive Expression ◽  
Lymphoid Cells ◽  
Interleukin 4 ◽  
B Cell Differentiation ◽  
Fluorescent Intensity ◽  
B Cell Growth Factor ◽  
B Lineage

Interleukin-4 (IL-4) regulates multiple stages of the antigen-dependent phase of B-cell development. However, its precise role in regulating B lymphopoiesis in bone marrow is not as well defined. We examined whether surface IgM- normal and leukemic human B-cell precursors (BCP) expressed IL-4 receptors using biotinylated IL-4. Constitutive expression of IL-4 receptors was detected on both normal and leukemic BCP. A higher percentage of normal BCP (82% +/- 15%) expressed IL-4 receptors compared with leukemic BCP (44% +/- 8%). Using mean fluorescent intensity as an indicator of receptor level on the IL-4 receptor positive cells, normal (91 +/- 41) and leukemic (44 +/- 37) BCP expressed comparable numbers of receptors. IL-4 induced the expression of CD23 on 30% of the leukemic BCP cases examined. IL-4 induced CD23 on surface IgM+ fetal bone marrow lymphoid cells but not on the surface IgM- normal BCP, despite the presence of detectable receptors on the surface IgM- cells. IL-4 did not stimulate proliferation of normal BCP, nor could it enhance the effect of recombinant IL-7 or low molecular weight B-cell growth factor. However, IL-4 increased the expression of surface IgM and surface Ig kappa on in vitro differentiated pre-B cells. Our collective results identify no role for IL-4 in the proliferation of normal or leukemic BCP, but identify a role in the enhancement of surface Ig expression during pre- B to B-cell differentiation.

JunB inhibits proliferation and transformation in B-lymphoid cells

Blood ◽  
2003 ◽  
Vol 102 (12) ◽  
pp. 4159-4165 ◽  
Author(s):  
Agnieszka P. Szremska ◽  
Lukas Kenner ◽  
Eva Weisz ◽  
Rene G. Ott ◽  
Emmanuelle Passegué ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
B Cell ◽  
Transgenic Animals ◽  
Inhibitory Effect ◽  
Lymphoid Cells ◽  
Negative Regulator ◽  
Transgenic Cells ◽  
B Lymphoid

Abstract The activator protein 1 (AP-1) member JunB has recently been implicated in leukemogenesis. Here we surveyed human lymphoma samples for expression of JunB and other AP-1 members (c-Jun, c-Fos, Fra1, JunD). JunB was strongly expressed in T-cell lymphomas, but non-Hodgkin B-cell lymphomas do not or only weakly express JunB. We therefore asked whether JunB acted as a negative regulator of B-cell development, proliferation, and transformation. We used transgenic mice that expressed JunB under the control of the ubiquitin C promoter; these displayed increased JunB levels in both B- and T-lymphoid cells. JunB transgenic cells of B-lymphoid, but not of T-lymphoid, origin responded poorly to mitogenic stimuli. Furthermore, JunB transgenic cells were found to be less susceptible to the transforming potential of the Abelson oncogene in vitro. In addition, overexpression of JunB partially protected transgenic mice against the oncogenic challenge in vivo. However, transformed B cells eventually escaped from the inhibitory effect of JunB: the proliferative response was similar in explanted tumor-derived cells from transgenic animals and those from wild-type controls. Our results identify JunB as a novel regulator of B-cell proliferation and transformation. (Blood. 2003;102:4159-4165)

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