scholarly journals Recombinant Tumor Necrosis Factor Enhances the Locomotion of Memory and Naive B Lymphocytes From Human Tonsils Through the Selective Engagement of the Type II Receptor

Blood ◽  
1997 ◽  
Vol 90 (11) ◽  
pp. 4493-4501 ◽  
Author(s):  
Anna Corcione ◽  
Luciano Ottonello ◽  
Giuseppe Tortolina ◽  
Paola Tasso ◽  
Fabio Ghiotto ◽  
...  
Keyword(s):  
Cell Migration ◽  
B Cells ◽  
Tumor Necrosis Factor ◽  
B Cell ◽  
B Lymphocytes ◽  
Tumor Necrosis ◽  
Type I ◽  
Dependent Manner ◽  
Type Ii ◽  
Necrosis Factor

Recent studies performed in mice knocked out for the tumor necrosis factor (TNF ), the lymphotoxin-α, or the type I TNF receptor (R), genes have shown that these animals display gross defects in germinal center (GC) formation, suggesting that members of the TNF and TNFR superfamilies are involved in the control of B-cell migration. Based on these premises, we have here investigated the effects of human recombinant (r) TNF on the polarization and locomotion of tonsillar B cells. rTNF increased the spontaneous polarization and locomotion of unfractionated tonsillar B lymphocytes in a dose-dependent manner by inducing a true chemotactic response. Memory (IgD−, CD38−) and naive (IgD+, CD38−), but not GC (IgD−, CD38+) B cells purified from total tonsillar B lymphocytes, showed a significantly higher locomotion in the presence than in the absence of rTNF. Accordingly, type I and II TNF receptors (TNFRs) were detected by flow cytometry on the surface of memory and naive, but not GC, B lymphocytes. Blocking experiments with monoclonal antibodies to type I or II TNFR showed that rTNF enhanced the spontaneous chemotaxis of memory and naive B cells through the selective engagement of type II TNFR. Finally, the TNF gene was found to be expressed in memory, naive and GC B lymphocytes; the cytokine was released in culture supernatants from the three B-cell subsets after stimulation. These data may support the hypothesis that human TNF is involved in the paracrine and perhaps autocrine control of B-cell migration in secondary lymphoid tissues.

scholarly journals Recombinant Tumor Necrosis Factor Enhances the Locomotion of Memory and Naive B Lymphocytes From Human Tonsils Through the Selective Engagement of the Type II Receptor

Blood ◽  
1997 ◽  
Vol 90 (11) ◽  
pp. 4493-4501 ◽  
Author(s):  
Anna Corcione ◽  
Luciano Ottonello ◽  
Giuseppe Tortolina ◽  
Paola Tasso ◽  
Fabio Ghiotto ◽  
...  
Keyword(s):  
Cell Migration ◽  
B Cells ◽  
Tumor Necrosis Factor ◽  
B Cell ◽  
B Lymphocytes ◽  
Tumor Necrosis ◽  
Type I ◽  
Dependent Manner ◽  
Type Ii ◽  
Necrosis Factor

Abstract Recent studies performed in mice knocked out for the tumor necrosis factor (TNF ), the lymphotoxin-α, or the type I TNF receptor (R), genes have shown that these animals display gross defects in germinal center (GC) formation, suggesting that members of the TNF and TNFR superfamilies are involved in the control of B-cell migration. Based on these premises, we have here investigated the effects of human recombinant (r) TNF on the polarization and locomotion of tonsillar B cells. rTNF increased the spontaneous polarization and locomotion of unfractionated tonsillar B lymphocytes in a dose-dependent manner by inducing a true chemotactic response. Memory (IgD−, CD38−) and naive (IgD+, CD38−), but not GC (IgD−, CD38+) B cells purified from total tonsillar B lymphocytes, showed a significantly higher locomotion in the presence than in the absence of rTNF. Accordingly, type I and II TNF receptors (TNFRs) were detected by flow cytometry on the surface of memory and naive, but not GC, B lymphocytes. Blocking experiments with monoclonal antibodies to type I or II TNFR showed that rTNF enhanced the spontaneous chemotaxis of memory and naive B cells through the selective engagement of type II TNFR. Finally, the TNF gene was found to be expressed in memory, naive and GC B lymphocytes; the cytokine was released in culture supernatants from the three B-cell subsets after stimulation. These data may support the hypothesis that human TNF is involved in the paracrine and perhaps autocrine control of B-cell migration in secondary lymphoid tissues.

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.

Tumor necrosis factor receptor-associated factor 1 gene overexpression in B-cell chronic lymphocytic leukemia: analysis of NF-κB/Rel–regulated inhibitors of apoptosis

Blood ◽  
2002 ◽  
Vol 100 (10) ◽  
pp. 3749-3756 ◽  
Author(s):  
Gerd Munzert ◽  
Dieter Kirchner ◽  
Heike Stobbe ◽  
Lothar Bergmann ◽  
Roland M. Schmid ◽  
...  
Keyword(s):  
B Cells ◽  
Chronic Lymphocytic Leukemia ◽  
Tumor Necrosis Factor ◽  
B Cell ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Lymphocytic Leukemia ◽  
Inhibitors Of Apoptosis ◽  
Necrosis Factor ◽  
Cell Chronic Lymphocytic Leukemia

B-cell chronic lymphocytic leukemia (B-CLL) is characterized by a resistance toward apoptosis-inducing agents. Nuclear factor-κB (NF-κB)/Rel has been shown to regulate the expression of antiapoptotic genes, such as members of the inhibitor of apoptosis protein (IAP) and tumor necrosis factor receptor-associated factor (TRAF) gene families. Expression and regulation of NF-κB/Rel–dependent inhibitors of apoptosis have not been collectively studied in B-CLL. We examined expression of known NF-κB/Rel–regulated antiapoptotic genes by RNAse protection assay, real-time polymerase chain reaction, and immunoblotting in patients with B-CLL. TRAF1 and to a lesser extent TRAF2 were overexpressed in B-CLL lymphocytes as compared with normal CD19+ B cells. TRAF1 overexpression did not correlate with markers of disease progression or overall survival. Furthermore, we found high constitutive expression of the IAP genes c-IAP-1, c-IAP-2, and XIAP both in normal and B-CLL lymphocytes. Focusing on the regulation of TRAF1, NF-κB/Rel activity in B-CLL nuclear extracts was shown to bind to TRAF1 promoter elements. However, IκB kinase (IKK) activity was not increased in CLL lymphocytes as compared with normal CD19+ B cells. The known IKK inhibitor sulfasalazine did not compromise TRAF1 expression. Thus, although our study revealed a common expression pattern of NF-κB/Rel–regulated inhibitors of apoptosis, our findings indicate an IKK-independent regulation of TRAF1 in B-CLL.

Levels of soluble receptors for tumor necrosis factor type I and type II in paired synovial fluids of arthritis patients

1993 ◽  
Vol 13 (3) ◽  
pp. 117-119 ◽  
Author(s):  
A. M. M. Miltenburg ◽  
D. Aderka ◽  
J. M. van Laar ◽  
D. Wallach ◽  
F. C. Breedveld
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Type I ◽  
Type Ii ◽  
Soluble Receptors ◽  
Synovial Fluids ◽  
Factor Type ◽  
Necrosis Factor

scholarly journals Coregulation of the APO-1 antigen with intercellular adhesion molecule- 1 (CD54) in tonsillar B cells and coordinate expression in follicular center B cells and in follicle center and mediastinal B-cell lymphomas

Blood ◽  
1993 ◽  
Vol 81 (8) ◽  
pp. 2067-2075 ◽  
Author(s):  
P Moller ◽  
C Henne ◽  
F Leithauser ◽  
A Eichelmann ◽  
A Schmidt ◽  
...  
Keyword(s):  
B Cells ◽  
Tumor Necrosis Factor ◽  
B Cell ◽  
Adhesion Molecule ◽  
Tumor Necrosis ◽  
Plasma Cells ◽  
Intercellular Adhesion Molecule ◽  
Cross Linking ◽  
Intercellular Adhesion Molecule 1 ◽  
Necrosis Factor

Abstract APO-1 is a 48-Kd transmembrane glycoprotein identical to the Fas antigen and belongs to the nerve growth factor (NGF)/tumor necrosis factor (TNF) receptor family of surface molecules. Cross-linking of APO- 1 induces apoptotic cell death in sensitive cells. We show here that APO-1 is an activation molecule on B cells. It was induced/enhanced on dense and buoyant tonsillar B cells, respectively, through surface Ig cross-linking in combination with interleukin-2 or by interferon-gamma together with tumor necrosis factor-alpha. These conditions also increased the amount of intercellular adhesion molecule-1 (CD54) on these cells. Epstein-Barr virus transformants of peripheral B cells coexpressed APO-1 and CD54 at very high levels. Immunohistologically, Apo-1 was detectable at low levels in a subpopulation of follicle center B blasts and, at higher levels, in sinusoidal B cells. APO-1 was undetectable in follicular mantle B cells and plasma cells. In isolated tonsillar B cells, APO-1 was expressed in CD10+ follicle center cells. In acute B lymphoblastic leukemia, chronic B lymphocytic leukemia, and Burkitt's lymphomas, APO-1 and CD54 molecules were immunohistochemically undetectable. Coordinate expression of these antigens was found in mediastinal B-cell lymphomas. The mode of APO-1 and CD54 expression was correlated in follicle center cell lymphomas (P < .0019), but less stringently in hairy cell leukemia. No association was found in plasmacytomas. This was in line with the differential expression of these molecules found in reactive plasma cells. Expression of APO-1 in B cells of different stages of differentiation and, correspondingly, in certain B-cell neoplasias might suggest a role of this molecule in the induction of B-cell apoptosis. This function might be influenced by CD54 and CD54-mediated signals.

Decreased expression of tumor necrosis factor family receptors involved in humoral immune responses in preterm neonates

Blood ◽  
2007 ◽  
Vol 110 (8) ◽  
pp. 2948-2954 ◽  
Author(s):  
Kulwant Kaur ◽  
Shimul Chowdhury ◽  
Neil S. Greenspan ◽  
John R. Schreiber
Keyword(s):  
B Cells ◽  
Tumor Necrosis Factor ◽  
B Cell ◽  
Tumor Necrosis ◽  
Antibody Responses ◽  
Preterm Neonates ◽  
Older Children ◽  
Humoral Immune ◽  
Encapsulated Bacteria ◽  
Necrosis Factor

AbstractNeonates have an increased rate of infection with encapsulated bacteria compared with older children and adults because of diminished antibody responses to T-independent (TI) antigens such as bacterial polysaccharides. Because the interactions of tumor necrosis factor (TNF) family ligands BAFF and APRIL with the TNF family receptors (TNFRs) TACI, BCMA, and BAFF-R are crucial to TI antibody responses, we measured the expression of these receptors on adult and cord blood–derived term and preterm neonatal B cells. Preterm neonatal B cells expressed less TACI, BCMA, and BAFF-R compared with adult B cells and had significantly less proliferation compared with adult B cells after stimulation with human recombinant BAFF and anti-IgM in an assay in which TACI-Fc fusion protein inhibits B-cell proliferation. In addition, neonatal dendritic cells had diminished expression of B7–1, B7–2, and CD40 compared with adult cells. Finally, neonatal B cells, particularly preterm B cells, exhibited markedly decreased production of IgG and IgA in response to CD40L and IL-10. Overall, this study shows that maturational delay in TNFR expression particularly by preterm neonatal B cells may interfere with effective antibody responses to TI antigens, cognate T- and B-cell interactions and normal isotype switching.

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