IL-24 sensitizes tumor cells to TLR3-mediated apoptosis

Weiss, René; Sachet, Monika; Zinngrebe, Julia; Aschacher, Thomas; Krainer, Michael; Hegedűs, Balázs; Walczak, Henning; Bergmann, Michael

doi:10.1038/cdd.2013.15

Cited by 30 publications

(20 citation statements)

References 48 publications

(64 reference statements)

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“…Related to this matter, poly(I:C)-induced cell death was previously shown to be mediated by a platform containing Caspase-8, RIP1, cIAPs, TRIF, and TLR3 (Estornes et al, 2012; Weiss et al, 2013). In addition, cIAPs have been identified to prevent formation of a poly(I:C)-induced signaling platform termed Ripoptosome consisting of RIP1 as its core component, Caspase-8, and TRIF (Feoktistova et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

LUBAC deficiency perturbs TLR3 signaling to cause immunodeficiency and autoinflammation

Zinngrebe

Rieser

Taraborrelli

et al. 2016

Journal of Experimental Medicine

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Section: Discussionmentioning

confidence: 99%

LUBAC deficiency perturbs TLR3 signaling to cause immunodeficiency and autoinflammation

Zinngrebe

Rieser

Taraborrelli

et al. 2016

Journal of Experimental Medicine

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“…TLR3-induced apoptosis can further be regulated by cytokines themselves. For example, interleukin-24, a type I IFN-induced cytokine, promoted TLR3-mediated apoptosis via the blockage of translation leading to a loss of the short-lived protein cFLIP in tumour cells [5]. TLR3-mediated apoptosis is further dependent on the balance of BCL2 family members as downregulation of MCL1 facilitates TLR3-mediated apoptosis [6].…”

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confidence: 99%

Initiation and execution mechanisms of necroptosis: an overview

2017

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Necroptosis is a form of regulated cell death, which is induced by ligand binding to TNF family death domain receptors, pattern recognizing receptors and virus sensors. The common feature of these receptor systems is the implication of proteins, which contain a receptor interaction protein kinase (RIPK) homology interaction motif (RHIM) mediating recruitment and activation of receptor-interacting protein kinase 3 (RIPK3), which ultimately activates the necroptosis executioner mixed lineage kinase domain-like (MLKL). In case of the TNF family members, the initiator is the survival- and cell death-regulating RIPK1 kinase, in the case of Toll-like receptor 3/4 (TLR3/4), a RHIM-containing adaptor, called TRIF, while in the case of Z-DNA-binding protein ZBP1/DAI, the cytosolic viral sensor itself contains a RHIM domain. In this review, we discuss the different protein complexes that serve as nucleation platforms for necroptosis and the mechanism of execution of necroptosis. Transgenic models (knockout, kinase-dead knock-in) and pharmacologic inhibition indicate that RIPK1, RIPK3 or MLKL are implicated in many inflammatory, degenerative and infectious diseases. However, the conclusion of necroptosis being solely involved in the etiology of diseases is blurred by the pleiotropic roles of RIPK1 and RIPK3 in other cellular processes such as apoptosis and inflammasome activation.

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“…The lymphoma cells after poly (I:C) treatment were characterized by rapid apoptosis that required a caspase cascade activated by TRIF and NF-κB. Although it has been reported that poly (I:C) can induce apoptosis in several tumor cell types including head and neck cancer, lung cancer, prostate cancer, breast cancer and others 3 , 6 , 8 – 10 , 22 , 23 . Moreover, Kalai et al .…”

Section: Discussionmentioning

confidence: 99%

Double-stranded RNA induces chicken T-cell lymphoma apoptosis by TRIF and NF-κB

Zou

Ruan

et al. 2017

Sci Rep

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Toll-like receptor-3 (TLR3), a member of the pathogen recognition receptor family, has been reported to activate immune response and to exhibit pro-apoptotic activity against some tumor cells. However it is unclear whether TLR3 has same function against chicken lymphoma. In this paper we investigated the effect of TLR3 activation on a Marek’s disease lymphoma-derived chicken cell line, MDCC-MSB1. The TLR3 agonist poly (I:C) activated TLR3 pathway and inhibited tumor cells proliferation through caspase-dependent apoptosis. Using pharmacological approaches, we found that an interferon-independent mechanism involving Toll-IL-1-receptor domain-containing adapter-inducing IFN-α (TRIF) and nuclear factor κB (NF-κB) causes the apoptosis of MDCC-MSB1 cells. This is the first report about the function of TLR3 in chicken T-cell lymphoma, especially in signal pathway. The mechanisms underlying TLR3-mediated apoptosis may contribute to the development of new drug to treat lymphomas and oncovirus infections.

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IL-24 sensitizes tumor cells to TLR3-mediated apoptosis

Cited by 30 publications

References 48 publications

LUBAC deficiency perturbs TLR3 signaling to cause immunodeficiency and autoinflammation

LUBAC deficiency perturbs TLR3 signaling to cause immunodeficiency and autoinflammation

Initiation and execution mechanisms of necroptosis: an overview

Double-stranded RNA induces chicken T-cell lymphoma apoptosis by TRIF and NF-κB

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IL-24 sensitizes tumor cells to TLR3-mediated apoptosis

Cited by 30 publications

References 48 publications

­­LUBAC deficiency perturbs TLR3 signaling to cause immunodeficiency and autoinflammation

­­LUBAC deficiency perturbs TLR3 signaling to cause immunodeficiency and autoinflammation

Initiation and execution mechanisms of necroptosis: an overview

Double-stranded RNA induces chicken T-cell lymphoma apoptosis by TRIF and NF-κB

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LUBAC deficiency perturbs TLR3 signaling to cause immunodeficiency and autoinflammation

LUBAC deficiency perturbs TLR3 signaling to cause immunodeficiency and autoinflammation