TRAIL receptor mediates inflammatory cytokine release in an NF-κB-dependent manner

Tang, Wanhu; Wang, Weimin; Zhang, Yaxi; Liu, Shilian; Liu, Yanxin; Zheng, Dexian

doi:10.1038/cr.2009.57

Cited by 48 publications

(38 citation statements)

References 34 publications

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“…As shown in Figure 4, NF-κB activity was activated in DR4 over-expressed cells, which was consistent with our previous report [11]. However, the activity of NF-κB was inhibited in PRMT5 over-expressed cells.…”

Section: Prmt5 Inhibits Nf-κb Activitysupporting

confidence: 82%

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PRMT5 suppresses DR4-mediated CCL20 release via NF-κB pathway

et al. 2012

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Construct expression vectors of pCMV-DR4-HA and pCMV-PRMT5-Flag, and transfect them into HEK293 cells to identify the interaction between TRAIL-R1 and PRMT5 and the molecular mechanism underlying DR4-mediated inhibition of chemokine CCL20 release via TRAIL receptor 1 (DR4). Inflammatory cytokine was detected by RT-PCR and ELISA after TRAIL-R1 and/or PRMT5 transfection, respectively. NF-κB activity was detected by Dual Luciferase Reporter Gene Assay. ERK1/2 phosphorylation was analyzed by Western blot. PRMT5 could inhibit DR4-activated NF-κB activity and ERK1/2 phosphorylation. PRMT5 could inhibit NF-κB activition, ERK1/2 phosphorylation as well as CCL20 secretion via binding with DR4 in HEK293 cell, suggesting that PRMT5 may involve in DR4 dependent immune regulation. TRAIL, PRMT5, cytokine, CCL20 Citation:Wang D S, Liu D, Gao J, et al. PRMT5 suppresses DR4-mediated CCL20 release via NF-κB pathway.

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Section: Prmt5 Inhibits Nf-κb Activitysupporting

confidence: 82%

“…There are some reports indicating that TRAIL induces IL-8 and MCP-1 expression in certain cell lines. Our previous study shows that TRAIL promotes the release of CCL20 through activating the NF-κB pathway [10,11]. Overexpression of DR4 can also cause the secretion of CCL20 by similar mechanism.…”

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confidence: 99%

PRMT5 suppresses DR4-mediated CCL20 release via NF-κB pathway

et al. 2012

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“…We also observed statistically significant associations with NHL for levels of the proinflammatory cytokines TNF-a, IL-16, 29 and TRAIL, 30 as well as for amylin, a polypeptide secreted by pancreatic B-cells involved in glycemic regulation. 31 However, these analytes were no longer associated with NHL after adjustment for BCA-1, sTNFR2, and sVEGFR2.…”

Section: Org Frommentioning

confidence: 68%

A prospective study of 67 serum immune and inflammation markers and risk of non-Hodgkin lymphoma

Purdue

Hofmann

Kemp

et al. 2013

Blood

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Key Points• Elevated levels of BCA-1, sTNFR2, and sVEGFR2 are associated with increased risk for NHL several years after blood collection. ), soluble tumor necrosis factor receptor 2 (sTNFR2; OR, 3.4; 95% CI, 2.0-5.8; P trend 5 1.1 3 10 26 ), and soluble vascular endothelial growth factor receptor 2 (sVEGFR2; OR, 2.3; 95% CI, 1.4-3.9; P trend 5 .0005) that remained significant after Bonferroni correction, simultaneous model adjustment, and restriction to cases diagnosed 8 to 13 years after blood collection. Associations with other markers were observed, although none remained associated with NHL after adjustment for BCA-1, sTNFR2, and sVEGFR2. Our findings suggest that circulating BCA-1, sTNFR2, and sVEGFR2 are associated with NHL risk well in advance of diagnosis. Additional research is needed to replicate these findings and elucidate the underlying biologic mechanisms. (Blood. 2013;122(6):951-957)

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“…TRAIL induces apoptosis and activates the transcription factor NF-kB (1,10). The TRAIL/TRAILR system is implicated in immune regulation and antitumor immunity (11,12).…”

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confidence: 99%

Dual Effects of TRAIL in Suppression of Autoimmunity: The Inhibition of Th1 Cells and the Promotion of Regulatory T Cells

Ikeda

Hirata

Fukushima

et al. 2010

The Journal of Immunology

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TRAIL is known to play a pivotal role in the inhibition of autoimmune disease. We previously demonstrated that administration of dendritic cells engineered to express TRAIL and myelin-oligodendrocyte glycoprotein reduced the severity of experimental autoimmune encephalomyelitis and suggested that CD4+CD25+ regulatory T cells (Tregs) were involved in mediating this preventive effect. In the current study, we investigated the effect of TRAIL on Tregs, as well as conventional T cells, using TRAIL-deficient mice. Upon induction of experimental autoimmune encephalomyelitis, TRAIL-deficient mice showed more severe clinical symptoms, a greater frequency of IFN-γ–producing CD4+ T (Th1) cells, and a lower frequency of CD4+Foxp3+ Tregs than did wild-type mice. In vitro, conventional T cells stimulated by bone marrow-derived dendritic cells (BM-DCs) from TRAIL-deficient mice showed a greater magnitude of proliferation than did those stimulated by BM-DCs from wild-type mice. In contrast, TRAIL expressed on the stimulator BM-DCs enhanced the proliferative response of CD4+CD25+ Tregs in the culture. The functional TRAILR, mouse death receptor 5 (mDR5), was expressed in conventional T cells and Tregs upon stimulation. In contrast, the decoy receptor, mDc-TRAILR1, was slightly expressed only on CD4+CD25+ Tregs. Therefore, the distinct effects of TRAIL may be due to differences in the mDc-TRAILR1 expression or the signaling pathways downstream of mouse death receptor 5 between the two T cell subsets. Our data suggest that TRAIL suppresses autoimmunity by two mechanisms: the inhibition of Th1 cells and the promotion of Tregs.

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TRAIL receptor mediates inflammatory cytokine release in an NF-κB-dependent manner

Cited by 48 publications

References 34 publications

PRMT5 suppresses DR4-mediated CCL20 release via NF-κB pathway

PRMT5 suppresses DR4-mediated CCL20 release via NF-κB pathway

A prospective study of 67 serum immune and inflammation markers and risk of non-Hodgkin lymphoma

Dual Effects of TRAIL in Suppression of Autoimmunity: The Inhibition of Th1 Cells and the Promotion of Regulatory T Cells

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