scholarly journals Costimulation of mast cells by 4-1BB, a member of the tumor necrosis factor receptor superfamily, with the high-affinity IgE receptor

Blood ◽  
2005 ◽  
Vol 106 (13) ◽  
pp. 4241-4248 ◽  
Author(s):  
Hajime Nishimoto ◽  
Seung-Woo Lee ◽  
Hong Hong ◽  
Karen G. Potter ◽  
Mari Maeda-Yamamoto ◽  
...  
Keyword(s):  
Mast Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Cytokine Production ◽  
Immunoglobulin E ◽  
Tumor Necrosis Factor Receptor ◽  
Protein Levels ◽  
High Affinity ◽  
High Affinity Receptor ◽  
Necrosis Factor

Mast cells are the major effector-cell type for immediate hypersensitivity and other forms of allergic reactions. Expression of 4-1BB, a member of the tumor necrosis factor receptor superfamily, is induced at mRNA and protein levels on stimulation through the high-affinity receptor for immunoglobulin E (IgE; FcϵRI). In this study, we present evidence that agonistic anti-4-1BB antibodies can enhance FcϵRI-induced cytokine production and secretion. Consistent with this, 4-1BB-deficient mast cells exhibit reduced degranulation and cytokine production on FcϵRI stimulation. Analysis of 4-1BB ligand (4-1BBL)-deficient cells supported this notion. As a potential mechanism for these defects, we identified a defect in Ca2+ flux induced by FcϵRI stimulation. The defective Ca2+ flux could be accounted for by the reduced activity of Lyn/Btk/phospholipase C-γ2 pathway and constitutive interactions between 4-1BB and Lyn. Therefore, FcϵRI-inducible 4-1BB plays a costimulatory function together with FcϵRI stimulation.

Tumor Necrosis Factor (TNF)-Soluble High-Affinity Receptor Complex as a TNF Antagonist

2007 ◽  
Vol 322 (2) ◽  
pp. 822-828 ◽  
Author(s):  
Sean D. McKenna ◽  
Georg Feger ◽  
Christie Kelton ◽  
Meijia Yang ◽  
Vittoria Ardissone ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Receptor Complex ◽  
High Affinity ◽  
Tnf Antagonist ◽  
High Affinity Receptor ◽  
Affinity Receptor ◽  
Necrosis Factor

High-Affinity Interactions of Tumor Necrosis Factor Receptor-Associated Factors (TRAFs) and CD40 Require TRAF Trimerization and CD40 Multimerization

Biochemistry ◽  
1999 ◽  
Vol 38 (31) ◽  
pp. 10168-10177 ◽  
Author(s):  
Steven S. Pullen ◽  
Mark E. Labadia ◽  
Richard H. Ingraham ◽  
Sarah M. McWhirter ◽  
Daniel S. Everdeen ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Associated Factors ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
High Affinity ◽  
Necrosis Factor

scholarly journals Silencing of Tumor Necrosis Factor Receptor 1 by siRNA in EC109 Cells Affects Cell Proliferation and Apoptosis

2009 ◽  
Vol 2009 ◽  
pp. 1-6 ◽  
Author(s):  
Ma Changhui ◽  
Ma Tianzhong ◽  
Su Zhongjing ◽  
Chen Ling ◽  
Wang Ning ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Necrosis Factor ◽  
Cell Line ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Signal Transduction Pathway ◽  
Cascade Reactions ◽  
Protein Levels ◽  
Mediating Role ◽  
Necrosis Factor

Tumor necrosis factor receptor 1 (TNFR1) is a membrane receptor able to bind TNF-αor TNF-β. TNFR1 can suppress apoptosis by activating the NF-κB or JNK/SAPK signal transduction pathway, or it can induce apoptosis through a series of caspase cascade reactions; the particular effect may depend on the cell line. In the present study, we first showed that TNFR1 is expressed at both the gene and protein levels in the esophageal carcinoma cell line EC109. Then, by applying a specific siRNA, we silenced the expression of TNFR1; this resulted in a significant time-dependent promotion of cell proliferation and downregulation of the apoptotic rate. These results suggest that TNFR1 is strongly expressed in the EC109 cell line and that it may play an apoptosis-mediating role, which may be suppressed by highly activated NF-κB.

scholarly journals Tumor Necrosis Factor (TNF) Receptor Superfamily Member TACI Is a High Affinity Receptor for TNF Family Members APRIL and BLyS

2000 ◽  
Vol 275 (45) ◽  
pp. 35478-35485 ◽  
Author(s):  
Youmei Wu ◽  
Dana Bressette ◽  
Jeff A. Carrell ◽  
Thomas Kaufman ◽  
Ping Feng ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Family Members ◽  
Tnf Receptor ◽  
High Affinity ◽  
High Affinity Receptor ◽  
Affinity Receptor ◽  
Necrosis Factor

Polymorphic analysis of the high-affinity tumor necrosis factor receptor 2

1999 ◽  
Vol 54 (6) ◽  
pp. 585-591 ◽  
Author(s):  
P. Pantelidis ◽  
P.A. Lympany ◽  
P.J. Foley ◽  
G.c Fanning ◽  
K.I. Welsh ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
High Affinity ◽  
Necrosis Factor ◽  
Polymorphic Analysis

scholarly journals Increased Mortality and Dysregulated Cytokine Production in Tumor Necrosis Factor Receptor 1-Deficient Mice following Systemic Klebsiella pneumoniae Infection

2003 ◽  
Vol 71 (9) ◽  
pp. 4891-4900 ◽  
Author(s):  
Thomas A. Moore ◽  
Michelle L. Perry ◽  
Andrew G. Getsoian ◽  
Christine L. Monteleon ◽  
Anna L. Cogen ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Klebsiella Pneumoniae ◽  
Tumor Necrosis ◽  
Cytokine Production ◽  
Lymphocyte Subsets ◽  
Tumor Necrosis Factor Receptor ◽  
Tnf Α ◽  
Ifn Γ ◽  
Deficient Mice ◽  
Necrosis Factor

ABSTRACT A significant clinical complication of pulmonary infections with Klebsiella pneumoniae is peripheral blood dissemination, resulting in a systemic infection concurrent with the localized pulmonary infection. In this context, little is known about the role of tumor necrosis factor receptor 1 (TNFR1)-mediated innate immune responses during systemic Klebsiella infections. Mice lacking TNFR1 were significantly more susceptible to Klebsiella-induced mortality following intravenous inoculation. Bacterial clearance was impaired in TNFR1-deficient mice at early times following infection. Unexpectedly, bacterial burdens at the onset of mortality (days 2 to 3 postinfection) were not higher in mice lacking TNFR1. However, elevated production of liver-associated proinflammatory cytokines (interleukin-12, tumor necrosis factor alpha [TNF-α[, and gamma interferon [IFN-γ]) and chemokines (MIP-1α, MIP-2, and MCP-1) was observed within the first 24 h of infection. Additionally, excessive plasma-associated IFN-γ was also observed late in the course of infection (day 3). Spleen cells from day-3 infected TNFR1-deficient mice secreted markedly enhanced levels of IFN-γ when cultured in vitro. Additionally, there was a marked increase in the total number of activated lymphocyte subsets as indicated by CD69 upregulation. A notable exception was the sharp decrease in the frequency of splenic NK T cells in infected TNFR1 knockout (KO) mice. Anti-TNF-α therapy in TNFR1 KO mice significantly reduced chemokine production and liver injury. Combined, these data indicate a dysregulated antibacterial host response following intravenous Klebsiella infection in the absence of TNFR1 signaling, resulting in heightened cytokine production and hyperactivation of specific splenic lymphocyte subsets.

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