Modulation of Dendritic Cell Differentiation and Maturation by Decoy Receptor 3

Hsu, Tsui Ling; Chang, Yung Chi; Chen, Siu Ju; Liu, Yong Jun; Chiu, Allen W.; Chio, Chung-Ching; Chen, Lieping; Hsieh, Shie Liang

doi:10.4049/jimmunol.168.10.4846

Cited by 111 publications

(111 citation statements)

References 38 publications

(47 reference statements)

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“…Our previous reports on RANK and DcR3 have indicated additional players by these soluble receptors in the regulation of cell function, and confirmed the concept of reverse signaling. [33][34][35]58 We demonstrated that DcR3 could modulate the differentiation and maturation of DC from CD14 þ monocytes. 33 Moreover, DcR3 can suppress macrophage differentiation from monocytes, but enhance monocyte adhesion.…”

Section: Ns Indicates Nonspecific Bindingmentioning

confidence: 70%

“…[33][34][35]58 We demonstrated that DcR3 could modulate the differentiation and maturation of DC from CD14 þ monocytes. 33 Moreover, DcR3 can suppress macrophage differentiation from monocytes, but enhance monocyte adhesion. 34,35 The present observation that DcR3 can enhance osteoclast differentiation from monocyte lineages through activation of ERK and p38 MAPK further strengthens the significance of reverse signaling to modulate cell function.…”

Section: Ns Indicates Nonspecific Bindingmentioning

confidence: 70%

“…33 Recombinant DcR3 protein was cleaved from the recombinant DcR3-Fc fusion protein by papain as previously described. 32 …”

Section: Generation Of Dcr3 Proteinmentioning

confidence: 99%

“…22,31,32 Third, we recently observed novel actions of DcR3 in monocytes. These include: (i) the modulation of dendritic cells' (DCs) differentiation and maturation, skewing the immune response from Th1 to Th2, 33 (ii) the modulation of macrophage differentiation and impairment of macrophage function, 34 and (iii) the enhancement of monocyte adhesion. 35 These three actions of DcR3 in monocytes are triggered by reverse signalings, irrelevant to cytokine neutralization, and contributes to suppression of host antitumor immunity.…”

Section: Introductionmentioning

confidence: 99%

“…29,[36][37][38][39] Since our recent study suggested that DcR3, like other members of the TNFR superfamily, is capable of triggering 'reverse signaling' to modulate monocyte differentiation, [33][34][35] we are interested in this study to understand whether DcR3 has any effects in modulating osteoclastogenesis from monocytes/macrophages.…”

Section: Introductionmentioning

confidence: 99%

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Decoy receptor 3 (DcR3) induces osteoclast formation from monocyte/macrophage lineage precursor cells

Yang

Wang

Hsieh³

et al. 2004

Cell Death Differ

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Recent evidence indicates that the decoy receptor 3 (DcR3) of the TNF receptor superfamily, which initially though prevents cytokine responses of FasL, LIGHT and TL1A by binding and neutralization, can modulate monocyte function through reverse signaling. We show in this work that DcR3 can induce osteoclast formation from human monocytes, murine RAW264.7 macrophages, and bone marrow cells. DcR3-differentiated cells exhibit characteristics unique for osteoclasts, including polynuclear giant morphology, bone resorption, TRAP, CD51/61, and MMP-9 expression. Consistent with the abrogation of osteoclastogenic effect of DcR3 by TNFRFc, DcR3 treatment can induce osteoclastogenic cytokine TNF-a release through ERK and p38 MAPK signaling pathways. We conclude that DcR3 via coupling reverse signaling of ERK and p38 MAPK and stimulating TNF-a synthesis is a critical regulator of osteoclast formation. This action of DcR3 might play an important role in significant osteoclastic activity in osteolytic bone metastases.

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Section: Ns Indicates Nonspecific Bindingmentioning

confidence: 70%

Section: Ns Indicates Nonspecific Bindingmentioning

confidence: 70%

“…33 Recombinant DcR3 protein was cleaved from the recombinant DcR3-Fc fusion protein by papain as previously described. 32 …”

Section: Generation Of Dcr3 Proteinmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Decoy receptor 3 (DcR3) induces osteoclast formation from monocyte/macrophage lineage precursor cells

Yang

Wang

Hsieh³

et al. 2004

Cell Death Differ

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TNF Superfamily

Cuzzocrea

2017

Inflammation - From Molecular and Cellular Mechanisms to the Clinic

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LIGHT (TNFSF14), a novel mediator of bone resorption, is elevated in rheumatoid arthritis

Edwards¹,

Sun²,

Locklin³

et al. 2006

Arthritis & Rheumatism

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Objective. Human osteoclast formation from mononuclear phagocyte precursors involves interactions between tumor necrosis factor (TNF) ligand superfamily members and their receptors. LIGHT is a transmembrane protein expressed and shed from the surface of activated T cells. Since activated T cells have been implicated in osteoclastogenesis in rheumatoid arthritis (RA), this study sought to determine whether LIGHT can regulate RANKL/cytokine-induced osteoclast formation, to identify the mechanism by which LIGHT influences osteoclastogenesis, and to investigate the presence of LIGHT in the serum of RA patients.Methods. The effect of LIGHT on human and murine osteoclast formation was assessed in the presence and absence of neutralizing reagents to known osteoclastogenic factors. Serum levels of LIGHT in RA patients were measured by enzyme-linked immunosorbent assay.Results. In the presence and absence of RANKL, LIGHT induced osteoclast formation from both human peripheral blood mononuclear cells and murine macrophage precursors, in a dose-dependent manner, whereas no inhibition was observed by adding osteoprotegerin, RANK:Fc, TNF␣, or interleukin-8 or by blocking the LIGHT receptors herpesvirus entry mediator or lymphotoxin ␤ receptor. However, formation of osteoclasts was significantly decreased by the soluble decoy receptor for LIGHT, DcR3, and by blocking antibodies to the p75 component of the TNF receptor. A significant increase in LIGHT levels in the serum of RA patients compared with normal controls was also noted.Conclusion. Our results indicate that LIGHT promotes RANKL-mediated osteoclastogenesis and that it can induce osteoclast formation by a mechanism independent of RANKL. The increased concentration of LIGHT in patients with RA raises the possibility that LIGHT may play a role in immunopathogenic conditions that are associated with localized or systemic bone loss.Osteoclasts are multinucleated cells that specifically function in lacunar bone resorption (1). Osteoclast differentiation from hematopoietic and circulating precursors requires the presence of macrophage colonystimulating factor (M-CSF) and the receptor activator for nuclear factor B ligand, RANKL (2-5). RANKL is a tumor necrosis factor (TNF) superfamily member that is expressed by osteoblasts and T cells and interacts with RANK on osteoclast precursors (5-8). Osteoprotegerin (OPG) acts as a decoy receptor for RANKL and blocks RANKL-mediated osteoclast differentiation and stimulation of osteoclast-resorbing activity (9,10). Although TNF␣ has also been shown to promote osteoclast formation by a RANKL-independent mechanism, the presence of TNF␣ results in considerably less lacunar resorption than that in RANKL-induced osteoclast formation (11,12).LIGHT (homologous to lymphotoxins exhibiting inducible expression and competing with herpes simplex virus glycoprotein D for herpesvirus entry mediator [HVEM], a receptor expressed by T lymphocytes) is a newly identified member of the TNF superfamily (TNFSF14), that is expressed by activated T

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Modulation of Dendritic Cell Differentiation and Maturation by Decoy Receptor 3

Cited by 111 publications

References 38 publications

Decoy receptor 3 (DcR3) induces osteoclast formation from monocyte/macrophage lineage precursor cells

Decoy receptor 3 (DcR3) induces osteoclast formation from monocyte/macrophage lineage precursor cells

TNF Superfamily

LIGHT (TNFSF14), a novel mediator of bone resorption, is elevated in rheumatoid arthritis

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