Inhibitors of apoptosis proteins (IAPs) are required for effective T-cell expansion/survival during antiviral immunity in mice

Blood ◽  
2014 ◽  
Vol 123 (5) ◽  
pp. 659-668 ◽  
Author(s):  
Ian E. Gentle ◽  
Isabel Moelter ◽  
Nadja Lechler ◽  
Sarah Bambach ◽  
Smiljka Vucikuja ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Cell Expansion ◽  
Tumor Necrosis ◽  
Activated T Cells ◽  
Inhibitors Of Apoptosis ◽  
Key Points ◽  
Inhibitors Of Apoptosis Proteins ◽  
Apoptosis Proteins ◽  
Necrosis Factor

Key Points IAPs are required for survival and expansion of activated T cells. IAP antagonists sensitize to tumor necrosis factor (TNF)-induced cell death of activated T cells during viral infection.

scholarly journals T cell receptor-dependent cell death of T cell hybridomas mediated by the CD30 cytoplasmic domain in association with tumor necrosis factor receptor-associated factors.

1996 ◽  
Vol 183 (2) ◽  
pp. 669-674 ◽  
Author(s):  
S Y Lee ◽  
C G Park ◽  
Y Choi
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Tumor Necrosis Factor ◽  
T Cell Receptor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Cell Receptor ◽  
Cytoplasmic Domain ◽  
Activated T Cells ◽  
Necrosis Factor

CD30 is a member of the tumor necrosis factor superfamily and a surface marker for Hodgkin's disease. Normal activated T cells and several virally transformed T or B cell lines also show CD30 expression. The interaction of CD30 with its ligand induces cell death or proliferation, depending on the cell type. In this report we characterize the signals mediated by the intracellular domain of CD30 and show that, in combination with signal(s) transduced by the T cell receptor, the multimerization of CD30 cytoplasmic domain induces Fas(CD95)-independent cell death in T cell hybridomas. Deletion analysis shows that the COOH-terminal 66 amino acids of CD30 are required to induce cell death. Using the yeast two-hybrid system, we have identified that the same region of CD30 interacts with tumor necrosis factor receptor-associated factor (TRAF)1 and TRAF2. These results indicate that TRAF1 and/or TRAF2 play an important role in cell death in addition to their previously identified roles in cell proliferation.

scholarly journals Monocytes Treated with Human Immunodeficiency Virus Tat Kill Uninfected CD4+ Cells by a Tumor Necrosis Factor-Related Apoptosis-Induced Ligand-Mediated Mechanism

2003 ◽  
Vol 77 (12) ◽  
pp. 6700-6708 ◽  
Author(s):  
Yida Yang ◽  
Ilia Tikhonov ◽  
Tracy J. Ruckwardt ◽  
Mahmoud Djavani ◽  
Juan Carlos Zapata ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Cell Surface Expression ◽  
Monocyte Subset ◽  
Hiv Tat ◽  
Immunodeficiency Virus ◽  
Necrosis Factor

ABSTRACT The human immunodeficiency virus (HIV) Tat protein has a critical role in viral transcription, but this study focuses on its additional role as an extracellular effector of lymphocyte cell death. It is well known that Tat induces tumor necrosis factor-related apoptosis-induced ligand (TRAIL) in peripheral blood mononuclear cells (PBMC), and we show that the majority of TRAIL is produced by the monocyte subset of PBMC. Human monocytes and U937 monoblastoid cells did not take up soluble HIV Tat-86, as T cells did, yet produced more TRAIL than did T cells. TRAIL secretion was induced by Tat and by a cysteine-rich peptide of Tat but not by sulfhydryl-modified Tat toxoid. Although there was only a slight increase in cell surface expression of TRAIL on monocytes, sufficient TRAIL was secreted to be toxic for T cells. The cytotoxicity of Tat-stimulated monocyte medium could be blocked by a TRAIL-neutralizing antibody. T cells treated with Tat did not secrete enough TRAIL to mediate cell death in our assay. Remarkably, uninfected T cells are more susceptible to TRAIL than are HIV-infected T cells. The production of TRAIL by Tat-stimulated monocytes provides a mechanism by which HIV infection can destroy uninfected bystander cells.

Chlamydia trachomatis-infected macrophages induce apoptosis of activated T cells by secretion of tumor necrosis factor-? in vitro

2004 ◽  
Vol 193 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Michael C. Jendro ◽  
Frederik Fingerle ◽  
Tobias Deutsch ◽  
Andrea Liese ◽  
Lars K�hler ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Chlamydia Trachomatis ◽  
Tumor Necrosis ◽  
Activated T Cells ◽  
Necrosis Factor

scholarly journals Wortmannin inhibits translation of tumor necrosis factor-α in superantigen-activated T cells

1999 ◽  
Vol 11 (9) ◽  
pp. 1479-1489 ◽  
Author(s):  
Matilde Ramírez ◽  
Neus Fernández-Troy ◽  
Maria Buxadé ◽  
Ricardo P. Casaroli-Marano ◽  
Daniel Benítez ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Activated T Cells ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Activated T Cells Induce Macrophages To Produce NO and Control Leishmania major in the Absence of Tumor Necrosis Factor Receptor p55

2000 ◽  
Vol 68 (3) ◽  
pp. 1428-1434 ◽  
Author(s):  
Michelle Nashleanas ◽  
Phillip Scott
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Leishmania Major ◽  
Tumor Necrosis Factor Receptor ◽  
No Production ◽  
Activated T Cells ◽  
Necrosis Factor

ABSTRACT The ability to activate macrophages in vitro for nitric oxide production and killing of Leishmania major parasites is dependent on tumor necrosis factor, although L. major-infected mice lacking the TNF receptor p55 (TNFRp55−/− mice) or both the TNFRp55 and TNFRp75 (TNFRp55p75−/− mice) are able to produce NO in vivo and eliminate the parasites. Here we report that activated T cells cocultured with macrophages results in TNFR-independent activation sufficient to control parasites and that both CD40/CD40L and LFA-1 contribute to T-cell-mediated macrophage activation. Thus, anti-CD3-stimulated T cells activated TNFR-deficient macrophages, while T cells from CD40L−/− mice were partially defective in triggering NO production by TNFRp55p75−/− macrophages. Moreover, in the presence of gamma interferon, anti-CD40 monoclonal antibody (MAb) activated TNFR-deficient macrophages. Finally, MAb blockade of LFA-1 completely inhibited macrophage NO production. Our data indicate that T cells can activate macrophages in the absence of TNF, thus providing a mechanism for how TNFR-deficient mice can control intracellular pathogens.

scholarly journals Vaccine-Induced Tumor Necrosis Factor–Producing T Cells Synergize with Cisplatin to Promote Tumor Cell Death

2014 ◽  
Vol 21 (4) ◽  
pp. 781-794 ◽  
Author(s):  
Tetje C. van der Sluis ◽  
Suzanne van Duikeren ◽  
Suzanna Huppelschoten ◽  
Ekaterina S. Jordanova ◽  
Elham Beyranvand Nejad ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Tumor Cell ◽  
Tumor Necrosis ◽  
Tumor Cell Death ◽  
Promote Tumor Cell ◽  
Necrosis Factor
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