Modulation of TNFSF expression in lymphoid tissue inducer cells by dendritic cells activated with Toll-like receptor ligands

Han, Sin Suk; Koo, Ji Hye; Bae, Jing Yu; Kim, Soo Chan; Baik, Song; Kim, Mi Yeon

doi:10.5483/bmbrep.2011.44.2.129

Cited by 6 publications

(6 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…zymosan, LPS (Han et al, 2011) and short ragweed pollen (Li et al, 2011). Up-regulation of OX40L requires activation of the NF-κB pathway, which is also integral to the production of pro-inflammatory cytokines.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Activation of Toll-like Receptor-2 by Endogenous Matrix Metalloproteinase-2 Modulates Dendritic-Cell-Mediated Inflammatory Responses

et al. 2014

View full text Add to dashboard Cite

SUMMARY Matrix metalloproteinase-2 (MMP-2) is involved in several physiological mechanisms, including wound healing and tumor progression. We show that MMP-2 directly stimulates dendritic cells (DCs) to both up-regulate OX40L on the cell surface and secrete inflammatory cytokines. The mechanism underlying DC activation includes physical association with Toll-like receptor-2 (TLR2), leading to NF-κB activation, OX40L up-regulation on DCs and ensuing TH2 differentiation. Significantly, MMP-2 polarizes T cells towards type-2 responses in vivo, in a TLR2-dependent manner. MMP-2-dependent type-2 polarization may represent a key immune regulatory mechanism to protect against a broad array of disorders, such as inflammatory, infectious and autoimmune diseases, which can be hijacked by tumors to evade immunity.

show abstract

Section: Resultsmentioning

confidence: 99%

“…TSLP as well as TLR2 and TLR4 agonists can increase OX40L expression through NF-κB activation (Arima et al, 2010; Han et al, 2011; Ito et al, 2005; Li et al, 2011). Neither TSLP (Arima et al, 2010) nor TNFα (a control for NF-κB activation) induced OX40L up-regulation on moDCs (Fig S2).…”

Section: Resultsmentioning

confidence: 99%

Activation of Toll-like Receptor-2 by Endogenous Matrix Metalloproteinase-2 Modulates Dendritic-Cell-Mediated Inflammatory Responses

et al. 2014

View full text Add to dashboard Cite

show abstract

“…RANKL is an important protein for osteoclastogenesis that is expressed by many cell types, including osteoblasts; stromal, dendritic, synovial, periodontal ligament; B cells; some tumor cells; fibroblasts; odontoblasts; cementoblasts; ameloblasts; and activated lymphocytes . RANKL knockout mice demonstrate decreased osteoclast numbers, defective bone remodeling, severe osteopetrosis, and no tooth eruption .…”

Section: Discussionmentioning

confidence: 99%

RANKL Inhibitors Induce Osteonecrosis of the Jaw in Mice With Periapical Disease

Aghaloo

Cheong

Bezouglaia

et al. 2013

Journal of Bone and Mineral Research

112

View full text Add to dashboard Cite

Antiresorptive medications are essential in treating diseases of pathologic osteoclastic bone resorption, including bone cancer and osteoporosis. Bisphosphonates (BPs) are the most commonly used antiresorptives in clinical practice. Although inhibition of bone resorption is important in regulating unwanted malignant and metabolic osteolysis, BP treatment is associated with potential side effects, including osteonecrosis of the jaws (ONJ). Recently, non-BP antiresorptive medications targeting osteoclastic function and differentiation, such as denosumab, have entered the clinical arena. Denosumab treatment results in a similar rate of ONJ as BPs. Animal models of ONJ, using high-dose BP treatment in combination with tooth extraction or dental disease, provide valuable tools and insight in exploring ONJ pathophysiology. However, the ability of other antiresorptives to induce ONJ-like lesions in animal models has not been explored. Such studies would be beneficial in providing support for the role of osteoclast inhibition in ONJ pathogenesis versus a direct BP effect on oral tissues. Here, we tested the ability of the receptor activator of NF-kB ligand (RANKL) inhibitors RANK-Fc (composed of the extracellular domain of RANK fused to the fragment crystallizable [Fc] portion of immunoglobulin G [IgG]) and OPG-Fc (composed of the RANKL-binding domains of osteoprotegerin [OPG] linked to the Fc portion of IgG) to induce ONJ in mice in the presence of periapical disease, but in the absence of dental extractions. We demonstrate radiographic evidence of ONJ in RANK-Fc–treated and OPG-Fc–treated mice, including inhibition of bone loss, increased bone density, lamina dura thickening, and periosteal bone deposition. These findings closely resembled the radiographic appearance of an ONJ patient on denosumab treatment. Histologic examination revealed that RANK-Fc treatment and OPG-Fc treatment resulted in absence of osteoclasts, periosteal bone formation, empty osteocytic lacunae, osteonecrosis, and bone exposure. In conclusion, we have successfully induced ONJ in mice with periapical disease, using potent osteoclast inhibitors other than BPs. Our findings, coupled with ONJ animal models using high-dose BPs, suggest that osteoclast inhibition is pivotal to the pathogenesis of ONJ.

show abstract

“…CD30 (TNFRSF8) is a 130-kD membrane glycoprotein receptor, originally identified on Reed-Sternberg cells of Hodgkin's lymphoma (HL). As a member of the tumor necrosis factor receptor (TNFR) superfamily, it is preferentially expressed in developing and activated lymphocytes (16)(17)(18)(19)(20) as well as in many cancers, including HL, CTCL, anaplastic large cell lymphoma (ALCL), and mastocytosis (21)(22)(23). Members of the TNFR superfamily are classically associated with transducing death signals, but CD30 does not contain the death domain of other TNFRs (24).…”

Section: Introductionmentioning

confidence: 99%

Epigenetic therapy overcomes treatment resistance in T cell prolymphocytic leukemia

et al. 2015

View full text Add to dashboard Cite

T-cell prolymphocytic leukemia (T-PLL) is a rare, mature T-cell neoplasm with distinct features and an aggressive clinical course. Early relapse and short overall survival are commonplace. Use of the monoclonal anti-CD52 antibody alemtuzumab has improved the rate of complete remission and duration of response to over 50% and between 6–12 months, respectively. Despite this advance, without an allogeneic transplant, resistant relapse is inevitable. We report complete (7) and partial (1) remissions in eight patients receiving alemtuzumab and cladribine with or without an HDAC inhibitor. These data show that administration of epigenetic agents overcomes alemtuzumab resistance. We report epigenetically induced expression of the surface receptor protein CD30 in T-PLL. Subsequent treatment with the anti-CD30 antibody drug conjugate brentuximab vedotin overcame organ specific (skin) resistance to alemtuzumab. Our findings demonstrate activity of combination epigenetic and immunotherapy in the incurable illness T-PLL, particularly in the setting of prior alemtuzumab therapy.

show abstract

Modulation of TNFSF expression in lymphoid tissue inducer cells by dendritic cells activated with Toll-like receptor ligands

Cited by 6 publications

References 29 publications

Activation of Toll-like Receptor-2 by Endogenous Matrix Metalloproteinase-2 Modulates Dendritic-Cell-Mediated Inflammatory Responses

Activation of Toll-like Receptor-2 by Endogenous Matrix Metalloproteinase-2 Modulates Dendritic-Cell-Mediated Inflammatory Responses

RANKL Inhibitors Induce Osteonecrosis of the Jaw in Mice With Periapical Disease

Epigenetic therapy overcomes treatment resistance in T cell prolymphocytic leukemia

Contact Info

Product

Resources

About