The Role of Fasl/Fas Signaling Network in Infections and Tumorigenesis
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RANKL As a Novel EMT Marker 858 Cell Research (2008) 18:858-870
npg RANKL as a novel EMT marker 858 Cell Research (2008) 18:858-870. npg © 2008 IBCB, SIBS, CAS All rights reserved 1001-0602/08 $ 30.00 ORIGINAL ARTICLE www.nature.com/cr Receptor activator of NF-κB Ligand (RANKL) expression is associated with epithelial to mesenchymal transition in human prostate cancer cells Valerie A Odero-Marah1, Ruoxiang Wang1, Gina Chu1, Majd Zayzafoon2, Jianchun Xu1, Chunmeng Shi1, Fray F Marshall1, Haiyen E Zhau1, Leland WK Chung1 1Molecular Urology and Therapeutics Program, Department of Urology and Winship Cancer Institute, Emory University School of Medicine, 1365B Clifton Road, NE, Atlanta, GA 30322, USA; 2Department of Pathology, University of Alabamn, Birmingham, AL 35294, USA Epithelial-mesenchymal transition (EMT) in cancer describes the phenotypic and behavioral changes of cancer cells from indolent to virulent forms with increased migratory, invasive and metastatic potential. EMT can be induced by soluble proteins like transforming growth factor β1 (TGFβ1) and transcription factors including Snail and Slug. We uti- lized the ARCaPE/ARCaPM prostate cancer progression model and LNCaP clones stably overexpressing Snail to identify novel markers associated with EMT. Compared to ARCaPE cells, the highly tumorigenic mesenchymal ARCaPM and ARCaPM1 variant cells displayed a higher incidence of bone metastasis after intracardiac administration in SCID mice. ARCaPM and ARCaPM1 expressed mesenchymal stromal markers of vimentin and N-cadherin in addition to elevated levels of Receptor Activator of NF-κB Ligand (RANKL). We observed that both epidermal growth factor (EGF) plus TGFβ1 treatment and Snail overexpression induced EMT in ARCaPE and LNCaP cells, and EMT was associated with increased expression of RANKL protein. -
Multiple Interactions of the Cytosolic Polyproline Region of the CD95
FEBS 25561 FEBS Letters 509 (2001) 255^262 View metadata, citation and similar papers at core.ac.uk brought to you by CORE Multiple interactions of the cytosolic polyproline region ofprovided the by CD95 Elsevier - Publisher Connector ligand: hints for the reverse signal transduction capacity of a death factor1 Jennifer Wenzela;2, Ralf Sanzenbachera;2, Markus Ghadimia, Marc Lewitzkyb, Qingchun Zhouc, David R. Kapland, Dieter Kabelitza, Stephan M. Fellerb, Ottmar Janssena;* aInstitute for Immunology, Christian-Albrechts-University, MichaelisstraMe 5, 24105 Kiel, Germany bCell Signalling Laboratory, Imperial Cancer Research Fund, University of Oxford, Institute of Molecular Medicine, John Radcli¡e Hospital, Headington, Oxford, UK cInstitute of Organic Synthesis, Center China Normal University, 430079 Wuhan, PR China dDepartment of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA Received 19 September 2001; revised 7 November 2001; accepted 7 November 2001 First published online 20 November 2001 Edited by Giulio Superti-Furga regulate activation of CD4- and CD8-positive T cells in Abstract The CD95/Fas/Apo-1 ligand is expressed on activated lymphocytes, NK cells, platelets, certain immune-privileged cells vivo. Upon stimulation with T cell receptor (TCR) agonists and some tumor cells and induces apoptosis through the death in the presence of CD95, cell cycle progression of CD4-pos- receptor CD95/Fas/Apo-1. In murine T cells, membrane-bound itive cells was found to be inhibited [14^16], while CD8-pos- CD95L (Fas ligand) also acts as a costimulatory receptor to itive cells were activated to proliferate [13^16]. The molecular coordinate activation and function in vivo. -
RANK Interaction and Signaling − RANKL Structural and Functional
Structural and Functional Insights of RANKL −RANK Interaction and Signaling Changzhen Liu, Thomas S. Walter, Peng Huang, Shiqian Zhang, Xuekai Zhu, Ying Wu, Lucy R. Wedderburn, Peifu This information is current as Tang, Raymond J. Owens, David I. Stuart, Jingshan Ren and of October 1, 2021. Bin Gao J Immunol published online 14 May 2010 http://www.jimmunol.org/content/early/2010/05/14/jimmun ol.0904033 Downloaded from Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: by guest on October 1, 2021 http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published May 14, 2010, doi:10.4049/jimmunol.0904033 The Journal of Immunology Structural and Functional Insights of RANKL–RANK Interaction and Signaling Changzhen Liu,*,†,1 Thomas S. Walter,‡,1 Peng Huang,x Shiqian Zhang,{ Xuekai Zhu,*,† Ying Wu,*,† Lucy R. Wedderburn,‖ Peifu Tang,x Raymond J. Owens,‡ David I. Stuart,‡ Jingshan Ren,‡ and Bin Gao*,†,‖ Bone remodeling involves bone resorption by osteoclasts and synthesis by osteoblasts and is tightly regulated by the receptor activator of the NF-kB ligand (RANKL)/receptor activator of the NF-kB (RANK)/osteoprotegerin molecular triad. -
Human Melanoma-Reactive CD4+ and CD8+ CTL Clones Resist Fas
Human Melanoma-Reactive CD4+ and CD8+ CTL Clones Resist Fas Ligand-Induced Apoptosis and Use Fas/Fas Ligand-Independent Mechanisms for Tumor Killing This information is current as of September 29, 2021. Licia Rivoltini, Marina Radrizzani, Paola Accornero, Paola Squarcina, Claudia Chiodoni, Arabella Mazzocchi, Chiara Castelli, Paolo Tarsini, Vincenzo Viggiano, Filiberto Belli, Mario P. Colombo and Giorgio Parmiani J Immunol 1998; 161:1220-1230; ; Downloaded from http://www.jimmunol.org/content/161/3/1220 References This article cites 60 articles, 32 of which you can access for free at: http://www.jimmunol.org/content/161/3/1220.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 29, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 1998 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Human Melanoma-Reactive CD41 and CD81 CTL Clones Resist Fas Ligand-Induced Apoptosis and Use Fas/Fas Ligand-Independent Mechanisms for Tumor Killing1 Licia Rivoltini,2* Marina Radrizzani,* Paola Accornero,* Paola Squarcina,* Claudia Chiodoni,* Arabella Mazzocchi,* Chiara Castelli,* Paolo Tarsini,* Vincenzo Viggiano,† Filiberto Belli,‡ Mario P. -
TRAIL and Cardiovascular Disease—A Risk Factor Or Risk Marker: a Systematic Review
Journal of Clinical Medicine Review TRAIL and Cardiovascular Disease—A Risk Factor or Risk Marker: A Systematic Review Katarzyna Kakareko 1,* , Alicja Rydzewska-Rosołowska 1 , Edyta Zbroch 2 and Tomasz Hryszko 1 1 2nd Department of Nephrology and Hypertension with Dialysis Unit, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] (A.R.-R.); [email protected] (T.H.) 2 Department of Internal Medicine and Hypertension, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] * Correspondence: [email protected] Abstract: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a pro-apoptotic protein showing broad biological functions. Data from animal studies indicate that TRAIL may possibly contribute to the pathophysiology of cardiomyopathy, atherosclerosis, ischemic stroke and abdomi- nal aortic aneurysm. It has been also suggested that TRAIL might be useful in cardiovascular risk stratification. This systematic review aimed to evaluate whether TRAIL is a risk factor or risk marker in cardiovascular diseases (CVDs) focusing on major adverse cardiovascular events. Two databases (PubMed and Cochrane Library) were searched until December 2020 without a year limit in accor- dance to the PRISMA guidelines. A total of 63 eligible original studies were identified and included in our systematic review. Studies suggest an important role of TRAIL in disorders such as heart failure, myocardial infarction, atrial fibrillation, ischemic stroke, peripheral artery disease, and pul- monary and gestational hypertension. Most evidence associates reduced TRAIL levels and increased TRAIL-R2 concentration with all-cause mortality in patients with CVDs. It is, however, unclear Citation: Kakareko, K.; whether low TRAIL levels should be considered as a risk factor rather than a risk marker of CVDs. -
Increased Expression of CD154 and FAS in SLE Patients’ Lymphocytes Maria Elena Manea, Ruediger B
Increased expression of CD154 and FAS in SLE patients’ lymphocytes Maria Elena Manea, Ruediger B. Mueller, Doru Dejica, Ahmed Sheriff, Georg Schett, Martin Herrmann, Peter Kern To cite this version: Maria Elena Manea, Ruediger B. Mueller, Doru Dejica, Ahmed Sheriff, Georg Schett, et al.. Increased expression of CD154 and FAS in SLE patients’ lymphocytes. Rheumatology International, Springer Verlag, 2009, 30 (2), pp.181-185. 10.1007/s00296-009-0933-4. hal-00568285 HAL Id: hal-00568285 https://hal.archives-ouvertes.fr/hal-00568285 Submitted on 23 Feb 2011 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Increased expression of CD154 and FAS in SLE patients’ lymphocytes Maria Elena Manea1‡, MD, Ruediger B. Mueller2,3‡, MD, Doru Dejica1, PhD, Ahmed Sheriff2, PhD, Georg Schett2, MD, Martin Herrmann2, PhD, Peter Kern4, MD 1 Department of Immunopathology. “Iuliu Hatieganu" University of Medicine and Pharmacy, Str Croitorilor no 19-21, 3400 Cluj-Napoca, Romania. 2 Department for Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nürnberg, Germany 3 Departement of Rheumatologie, Kantonsspital St. Gallen, Switzerland 4 Franz von Prümmer Klinik, Bahnhofstraße 16, 97769 Bad Brückenau, Germany ‡ both authors equally contributed to the work Address correspondence and reprint requests to: Ruediger B. -
The Roadmap of RANKL/RANK Pathway in Cancer
cells Review The Roadmap of RANKL/RANK Pathway in Cancer Sandra Casimiro 1,* , Guilherme Vilhais 2, Inês Gomes 1 and Luis Costa 1,3,* 1 Luis Costa Laboratory, Instituto de Medicina Molecular—João Lobo Antunes, Faculdade de Medicina da Universidade de Lisboa, 1649-028 Lisboa, Portugal; [email protected] 2 Faculdade de Medicina da Universidade de Lisboa, 1649-028 Lisboa, Portugal; [email protected] 3 Oncology Division, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, 1649-028 Lisboa, Portugal * Correspondence: [email protected] (S.C.); [email protected] (L.C.) Abstract: The receptor activator of the nuclear factor-κB ligand (RANKL)/RANK signaling pathway was identified in the late 1990s and is the key mediator of bone remodeling. Targeting RANKL with the antibody denosumab is part of the standard of care for bone loss diseases, including bone metastases (BM). Over the last decade, evidence has implicated RANKL/RANK pathway in hormone and HER2-driven breast carcinogenesis and in the acquisition of molecular and phenotypic traits associated with breast cancer (BCa) aggressiveness and poor prognosis. This marked a new era in the research of the therapeutic use of RANKL inhibition in BCa. RANKL/RANK pathway is also an important immune mediator, with anti-RANKL therapy recently linked to improved response to immunotherapy in melanoma, non-small cell lung cancer (NSCLC), and renal cell carcinoma (RCC). This review summarizes and discusses the pre-clinical and clinical evidence of the relevance of the RANKL/RANK pathway in cancer biology and therapeutics, focusing on bone metastatic disease, BCa onset and progression, and immune modulation. -
The Role of the Immune Checkpoint Modulator OX40 and Its Ligand in NK Cell Immunosurveillance and Acute Myeloid Leukemia
1 The role of the immune checkpoint modulator OX40 and its ligand in NK cell 2 immunosurveillance and acute myeloid leukemia 3 Running title: OX40-OX40L in NK cell immunosurveillance 4 Keywords: OX40, AML, NK cells, immunotherapy, checkpoint 5 Tina Nuebling*1, Carla Emilia Schumacher*1,2, Martin Hofmann3, Ilona Hagelstein1, Benjamin Joachim 6 Schmiedel1, Stefanie Maurer1, Birgit, Federmann4, Kathrin Rothfelder1, Malte Roerden2, Daniela Dörfel1,2, 7 Pascal Schneider5, Gundram Jung3, Helmut Rainer Salih1,2 8 1 9 Clinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German 10 Cancer Research Center (DKFZ), Heidelberg, Germany 2 11 Department of Hematology and Oncology, Eberhard Karls University, Tuebingen, Germany 3 12 Department of Immunology, Eberhard Karls University, Tuebingen, Germany 13 4 Department of Pathology, Eberhard Karls University, Tuebingen, Germany 14 5 Department of Biochemistry, Epalinges, Switzerland 15 16 *these authors contributed equally to this work 17 18 Corresponding Author: 19 Helmut R. Salih, M.D. 20 Clinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK) and German 21 Cancer Research Center (DKFZ) 22 Department of Hematology and Oncology, Eberhard Karls University 23 Otfried-Mueller Str. 10, 72076 Tuebingen, Germany 24 Phone: +49-7071-2983275; Fax: +49-7071-293671; Email: [email protected] 25 26 Funding: Supported by grants from the Deutsche Forschungsgemeinschaft (NU341/1-1, SA1360/7-3, 27 SFB685, project A07), Deutsche Krebshilfe (projects 111828 and 111134). PS is supported by grants from 28 the Swiss National Science Foundation. 29 Conflict-of-interest disclosure: The authors declare no potential conflicts of interest. 30 31 32 Text word count: 4347; Abstract word count: 238 33 5 figures, 2 tables, 4 supplementary figures 34 References: 50 1 35 Abstract 36 The TNF receptor family member OX40 promotes activation and proliferation of T cells, which 37 fuels present attempts to modulate this immune checkpoint to reinforce anti-tumor immunity. -
(Blys) on Diabetes-Related Periodontitis
ORIGINAL RESEARCH Immunology Preliminary findings on the possible role of B-lymphocyte stimulator (BLyS) on diabetes-related periodontitis Marx Haddley Ferreira Abstract: The possible role of B-cell growth and differentiation- DRUMOND(a) related cytokines on the pathogenesis of diabetes-related periodontitis Luciano Eduardo PUHL(a) has not been addressed so far. The aim of this study was to evaluate Poliana Mendes DUARTE(b) the effects of diabetes mellitus (DM) on the gene expression of Tamires Szeremeske de proliferation-inducing ligand (APRIL) and B-lymphocyte stimulator MIRANDA(c) (BLyS), two major cytokines associated to survival, differentiation Juliana Trindade and maturation of B cells in biopsies from gingival tissue with CLEMENTE-NAPIMOGA(a) periodontitis. Gingival biopsies were obtained from subjects with Daiane Cristina PERUZZO(a) periodontitis (n = 17), with periodontitis and DM (n = 19) as well as Elizabeth Ferreira MARTINEZ(a) from periodontally and systemically healthy controls (n = 10). Gene Marcelo Henrique NAPIMOGA(a) expressions for APRIL, BLyS, RANKL, OPG, TRAP and DC-STAMP were evaluated using qPCR. The expressions APRIL, BLyS, RANKL, (a) Faculdade São Leopoldo Mandic, Instituto OPG, TRAP and DC-STAMP were all higher in both periodontitis de Pesquisas São Leopoldo Mandic, groups when compared to the control group (p < 0.05). Furthermore, Campinas, SP, Brazil. the expressions of BLyS, TRAP and RANKL were significantly higher (b) University of Florida, College of Dentistry, in the subjects with periodontitis and DM when compared to those Department of Periodontology, Gainesville, FL, USA. with periodontitis alone (p < 0.05). The mRNA levels of BLyS correlated positively with RANKL in the subjects with periodontitis and DM (c) Guarulhos University, Dental Research Division, Department of Periodontology, São (p < 0.05). -
Multimeric Forms of 4-1BBL As Stimulators of T Cells for Adoptive Immunotherapy
Kornbluth et al. Journal for ImmunoTherapy of Cancer 2014, 2(Suppl 3):P246 http://www.immunotherapyofcancer.org/content/2/S3/P246 POSTERPRESENTATION Open Access Multimeric forms of 4-1BBL as stimulators of T cells for adoptive immunotherapy Richard S Kornbluth1*, Victoria Snarsky1, Geoffrey W Stone2 From Society for Immunotherapy of Cancer 29th Annual Meeting National Harbor, MD, USA. 6-9 November 2014 Members of the TNF SuperFamily of ligands (TNFSFs) Authors’ details 1Multimeric Biotherapeutics, Inc., La Jolla, CA, USA. 2University of Miami, have significant potential as immuno-oncology therapeu- Miller School of Medicine, Miami, FL, USA. tic agents. The TNFSFs are trimeric membrane proteins that can be cleaved into soluble single trimers. While Published: 6 November 2014 the soluble single trimers can be easily prepared and studied, they have little or no activity in vivo. This defi- ciency is caused by the need to cluster their cognate doi:10.1186/2051-1426-2-S3-P246 Cite this article as: Kornbluth et al.: Multimeric forms of 4-1BBL as receptors in the plane of the membrane in order to stimulators of T cells for adoptive immunotherapy. Journal for induce a supramolecular signaling complex on the cyto- ImmunoTherapy of Cancer 2014 2(Suppl 3):P246. plasmic side of the plasma membrane. For the TNFSF ligands, this requires that they be used as many-trimer multimers that mimic the natural expression of many trimers on the surface of stimulating cells. To meet this need, we prepared fusion proteins comprised of the extracellular domains of TNFSF ligands joined to a nat- ural protein that provides a multimerization scaffold. -
Belongs to the TNF Family a New Class of Reverse Signaling
A New Class of Reverse Signaling Costimulators Belongs to the TNF Family Mingyi Sun and Pamela J. Fink This information is current as J Immunol 2007; 179:4307-4312; ; of September 27, 2021. doi: 10.4049/jimmunol.179.7.4307 http://www.jimmunol.org/content/179/7/4307 References This article cites 85 articles, 38 of which you can access for free at: Downloaded from http://www.jimmunol.org/content/179/7/4307.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision http://www.jimmunol.org/ • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: by guest on September 27, 2021 http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2007 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. THE JOURNAL OF IMMUNOLOGY BRIEF REVIEWS A New Class of Reverse Signaling Costimulators Belongs to the TNF Family Mingyi Sun and Pamela J. Fink1 Recent evidence shows that many molecules of the TNF still remains unclear (7). The N-terminal cytoplasmic domains family serve as counter-receptors, inducing costimulation of most TNF family members are conserved across species but through reverse signals in addition to delivering signals not between family members, suggesting that the intracellular through their respective TNF receptors. -
CD95 Ligand - Death Factor and Costimulatory Molecule?
Cell Death and Differentiation (2003) 10, 1215–1225 & 2003 Nature Publishing Group All rights reserved 1350-9047/03 $25.00 www.nature.com/cdd Review CD95 ligand - death factor and costimulatory molecule? O Janssen*,1, J Qian1, A Linkermann1 and D Kabelitz1 Tissue and Cellular Expression of CD95L 1 Institute for Immunology, Medical Center Schleswig-Holstein, Campus Kiel, Michaelisstrasse 5, D-24105 Kiel, Germany The CD95 ligand (CD95L, Apo-1L, FasL, CD178) is a 281- * Corresponding author: O Janssen. Tel: þ 49-431-5973377; Fax: þ 49-431- amino-acid-containing type II transmembrane protein of the 5973335; E-mail: [email protected] TNF family of death factors (Figure 1).1 Its death-inducing function is best documented in the context of activation- Received 24.4.03; revised 12.6.03; accepted 20.6.03; published online 1 August 2003 induced cell death (AICD) in T cells.2 CD95L is expressed as a Edited by T Ferguson death factor in cytotoxic T lymphocytes (CTL) to kill virally infected or transformed target cells and in natural killer (NK) cells, where it is upregulated by CD16 engagement and 3 Abstract cytokines including IL-2 and IL-12. Similarly, high levels of intracellular CD95L have been detected in monocytic cells The CD95 ligand is involved as a death factor in the with an inducible release upon activation.4 Under physiologi- regulation of activation-induced cell death, establishment cal conditions, CD95L is implicated in the control of erythroid of immune privilege and tumor cell survival. In addition, differentiation,5 angiogenesis in the eye6 and skin home- 7 CD95L may serve as a costimulatory molecule for T-cell ostasis.