Roles for TNF-receptor associated factor 3 (TRAF3) in lymphocyte functions

Yi, Zuoan; Lin, Wai Wai; Stunz, Laura L.; Bishop, Gail A.

doi:10.1016/j.cytogfr.2013.12.002

Cited by 41 publications

(32 citation statements)

References 139 publications

(191 reference statements)

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“…These inhibitory effects on the TNFR2 cascade were blocked by treatment with LRP1 siRNA, suggesting that the LRP1 mediates inhibition of the TNF-α receptor-mediated cell death cascade. TNF-α can activate TNFR1 and TNFR2 receptor subtypes, both of which trigger cell death through similar signaling cascades (Leon et al, 2013; Trebicka et al, 2013; Yi et al, 2013). TNFR1 is most commonly associated with cell death in various different cell types, while TNFR2 has been more prominently linked to cell apoptosis in neural tissues (Chen and Palmer, 2013).…”

Section: Discussionmentioning

confidence: 99%

IGFBP-3 inhibits TNF-α production and TNFR-2 signaling to protect against Retinal Endothelial Cell Apoptosis

Zhang

Steinle

2014

Microvascular Research

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In models of diabetic retinopathy, insulin-like growth factor binding protein-3 (IGFBP-3) protects against tumor necrosis factors-alpha (TNF-α)-mediated apoptosis of retinal microvascular endothelial cells (REC), but the underlying mechanisms are unclear. Our current findings suggest that at least two discrete but complimentary pathways contribute to the protective effects of IGFBP-3; 1) IGFBP-3 directly activates the c-Jun kinase/tissue inhibitor of metalloproteinase-3/TNF-α converting enzyme (c-Jun/TIMP-3/TACE), pathway, which in turn inhibits TNF-α production; 2) IGFBP-3 acts through the IGFBP-3 receptor, low-density lipoprotein receptor-related protein 1 (LRP1), to inhibit signaling of TNF-α receptor 2 (TNFR2). Combined, these two IGFBP-3 pathways substantially reduce REC apoptosis and offer potential targets for the treatment of diabetic retinopathy.

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Section: Discussionmentioning

confidence: 99%

IGFBP-3 inhibits TNF-α production and TNFR-2 signaling to protect against Retinal Endothelial Cell Apoptosis

Zhang

Steinle

2014

Microvascular Research

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“…TRAF3 is a member of the TRAF families and ubiquitously expressed in most tissues and cell types, including brain, lung, heart, spleen, and liver 13,14. TRAF3 experiences interactions with various biological molecules, such as receptors, kinases, adaptors, and regulatory proteins, to exert its different biological functions 15.…”

Section: Introductionmentioning

confidence: 99%

miR-455 inhibits neuronal cell death by targeting TRAF3 in cerebral ischemic stroke

Yao

Tang

et al. 2016

NDT

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Ischemic stroke is one of the leading causes of brain disease, with high morbidity, disability, and mortality. MicroRNAs (miRNAs) have been identified as vital gene regulators in various types of human diseases. Accumulating evidence has suggested that aberrant expression of miRNAs play critical roles in the pathologies of ischemic stroke. Yet, the precise mechanism by which miRNAs control cerebral ischemic stroke remains unclear. In the present study, we explored whether miR-455 suppresses neuronal death by targeting TRAF3 in cerebral ischemic stroke. The expression levels of miR-455 and TRAF3 were detected by quantitative real-time polymerase chain reaction and Western blot. The role of miR-455 in cell death caused by oxygen–glucose deprivation (OGD) was assessed using Cell Counting Kit-8 (CCK-8) assay. The influence of miR-455 on infarct volume was evaluated in mouse brain after middle cerebral artery occlusion (MCAO). Bioinformatics softwares and luciferase analysis were used to find and confirm the targets of miR-455. The results showed that the expression levels of miR-455 significantly decreased in primary neuronal cells subjected to OGD and mouse brain subjected to MCAO. In addition, forced expression of miR-455 inhibited neuronal death and weakened ischemic brain infarction in focal ischemia-stroked mice. Furthermore, TRAF3 was proved to be a direct target of miR-455, and miR-455 could negatively suppress TRAF3 expression. Biological function analysis showed that TRAF3 silencing displayed the neuroprotective effect in ischemic stroke and could enhance miR-455-induced positive impact on ischemic injury both in vitro and in vivo. Taken together, miR-455 played a vital role in protecting neuronal cells from death by downregulating TRAF3 protein expression. These findings may represent a novel latent therapeutic target for cerebral ischemic stroke.

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“…TRAF3 also participates in signaling through Toll-like receptors (TLRs), as well as through the T cell antigen receptor (TCR) complex (1, 2). In addition, TRAF3 plays a role in mediating interleukin-17 (IL-17) receptor (IL-17R) and IL-2R signaling (3, 4).…”

Section: Introductionmentioning

confidence: 99%

“…In addition, TRAF3 plays a role in mediating interleukin-17 (IL-17) receptor (IL-17R) and IL-2R signaling (3, 4). Evidence is accumulating that the function of TRAF3 is highly receptor- and cell type–specific (1). Mice with a B cell–specific deletion of TRAF3 (B- Traf3 −/− mice) show a marked B cell survival advantage in the absence of increased proliferation (5, 6).…”

Section: Introductionmentioning

confidence: 99%

The adaptor protein TRAF3 inhibits interleukin-6 receptor signaling in B cells to limit plasma cell development

Lin

Stunz

et al. 2015

Sci. Signal.

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Tumor necrosis factor receptor–associated factor 3 (TRAF3) is an adaptor protein that inhibits signaling by CD40 and by the receptor for B cell–activating factor (BAFF) and negatively regulates homeostatic B cell survival. Loss-of-function mutations in TRAF3 are associated with human B cell malignancies, in particular multiple myeloma. The cytokine interleukin-6 (IL-6) supports the differentiation and survival of normal and neoplastic plasma cells. We found that mice with a deficiency in TRAF3 specifically in B cells (B-Traf3−/− mice) had about twice as many plasma cells as did their littermate controls. TRAF3-deficient B cells had enhanced responsiveness to IL-6, and genetic loss of IL-6 in B-Traf3−/− mice restored their plasma cell numbers to normal. TRAF3 inhibited IL-6 receptor (IL-6R)–mediated signaling by facilitating the association of PTPN22 (a nonreceptor protein tyrosine phosphatase) with the kinase Janus-activated kinase 1 (Jak1), which in turn blocked phosphorylation of the transcription factor STAT3 (signal transducer and activator of transcription 3). Consistent with these results, the number of plasma cells in the PTPN22-deficient mice was increased compared to that in the wild-type mice. Our findings identify TRAF3 and PTPN22 as inhibitors of IL-6R signaling in B cells and reveal a previously uncharacterized role for TRAF3 in the regulation of plasma cell differentiation.

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Roles for TNF-receptor associated factor 3 (TRAF3) in lymphocyte functions

Cited by 41 publications

References 139 publications

IGFBP-3 inhibits TNF-α production and TNFR-2 signaling to protect against Retinal Endothelial Cell Apoptosis

IGFBP-3 inhibits TNF-α production and TNFR-2 signaling to protect against Retinal Endothelial Cell Apoptosis

miR-455 inhibits neuronal cell death by targeting TRAF3 in cerebral ischemic stroke

The adaptor protein TRAF3 inhibits interleukin-6 receptor signaling in B cells to limit plasma cell development

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