Proinflammatory Cytokine Activation Is Linked to Apoptotic Mediator, Soluble Fas Level in Patients with Chronic Heart Failure
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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. -
(CS-ⅣA-Be), a Novel IL-6R Antagonist, Inhibits IL-6/STAT3
Author Manuscript Published OnlineFirst on February 29, 2016; DOI: 10.1158/1535-7163.MCT-15-0551 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Chikusetsusaponin Ⅳa butyl ester (CS-Ⅳa-Be), a novel IL-6R antagonist, inhibits IL-6/STAT3 signaling pathway and induces cancer cell apoptosis Jie Yang 1, 2, Shihui Qian 2, Xueting Cai 1, 2, Wuguang Lu 1, 2, Chunping Hu 1, 2, * Xiaoyan Sun1, 2, Yang Yang1, 2, Qiang Yu 3, S. Paul Gao 4, Peng Cao 1, 2 1. Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210028, China 2. Laboratory of Cellular and Molecular Biology, Jiangsu Province Academy of Traditional Chinese Medicine, Nanjing 210028, China 3. Shanghai Institute of Materia Medical, Chinese Academy of Sciences, Shanghai, 201203, China 4. Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY10065, USA Running title: CS-Ⅳa-Be, a novel IL-6R antagonist, inhibits IL-6/STAT3 Keywords: Chikusetsusaponin Ⅳ a butyl ester (CS- Ⅳ a-Be), STAT3, IL-6R, antagonist, cancer Grant support: P. Cao received Jiangsu Province Funds for Distinguished Young Scientists (BK20140049) grant, J. Yang received National Natural Science Foundation of China (No. 81403151) grant, and X.Y. Sun received National Natural Science Foundation of China (No. 81202576) grant. Corresponding author: Peng Cao Institute: Laboratory of Cellular and Molecular Biology, Jiangsu Province Academy of Traditional Chinese Medicine, Nanjing 210028, Jiangsu, China Mailing address: 100#, Shizi Street, Hongshan Road, Nanjing, Jiangsu, China Tel: +86-25-85608666 Fax: +86-25-85608666 Email address: [email protected] The first co-authors: Jie Yang and Shihui Qian The authors disclose no potential conflicts of interest. -
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. -
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. -
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. -
Interaction Apoptosis Mediated by Fas/Fas Ligand Osteoclast Formation In
Effect of IL-12 on TNF-α-Mediated Osteoclast Formation in Bone Marrow Cells: Apoptosis Mediated by Fas/Fas Ligand Interaction This information is current as of October 6, 2021. Hideki Kitaura, Noriko Nagata, Yuji Fujimura, Hitoshi Hotokezaka, Noriaki Yoshida and Koji Nakayama J Immunol 2002; 169:4732-4738; ; doi: 10.4049/jimmunol.169.9.4732 http://www.jimmunol.org/content/169/9/4732 Downloaded from References This article cites 54 articles, 29 of which you can access for free at: http://www.jimmunol.org/content/169/9/4732.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 • Fast Publication! 4 weeks from acceptance to publication by guest on October 6, 2021 *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 © 2002 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Effect of IL-12 on TNF-␣-Mediated Osteoclast Formation in Bone Marrow Cells: Apoptosis Mediated by Fas/Fas Ligand Interaction1 Hideki Kitaura,2* Noriko Nagata,*† Yuji Fujimura,*† Hitoshi Hotokezaka,* Noriaki Yoshida,* and Koji Nakayama† Recently, it has been found that differentiation into osteoclasts is induced by TNF-␣. -
Kcnorman 1.Pdf
A Computational Systems Approach to Elucidate New Mechanisms Involved in Progressive Lung Disease by Katy Norman A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Biomedical Engineering) in the University of Michigan 2020 Doctoral Committee: Assistant Professor Kelly Arnold, Chair Professor Jeffrey Curtis Professor Jennifer Linderman Professor Bethany Moore Professor David Sept Katy C. Norman [email protected] ORCID iD: 0000-0001-8841-0212 © Katy C. Norman 2020 Acknowledgements When I look back on myself in 2015 as I just entered the PhD program, I have to give a little laugh about all the surprises and changes that have happened along the way. I have grown more than I could ever have imagined – I have become so much more comfortable and confident in my communication skills, in my scientific skills, and in myself. These changes and this growth could not have happened without my huge support network, and I am honored to have the chance to thank everyone for what they have given me and for what they have helped me achieve. I would first like to thank my adviser, Kelly Arnold, for giving me a chance to try out computational systems biology research when I had absolutely no background in the field coming in. I appreciate how you were easily able to create a space where I felt comfortable to learn, to ask questions, and to make mistakes as I worked towards gaining expertise in this field. Thank you for always being there for me with extra support when my nerves were getting the best of me before big presentations or before a big deadline, and for supporting my involvement in activities outside of the lab as well. -
GP130 Cytokines in Breast Cancer and Bone
cancers Review GP130 Cytokines in Breast Cancer and Bone Tolu Omokehinde 1,2 and Rachelle W. Johnson 1,2,3,* 1 Program in Cancer Biology, Vanderbilt University, Nashville, TN 37232, USA; [email protected] 2 Vanderbilt Center for Bone Biology, Department of Medicine, Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA 3 Department of Medicine, Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA * Correspondence: [email protected]; Tel.: +1-615-875-8965 Received: 14 December 2019; Accepted: 29 January 2020; Published: 31 January 2020 Abstract: Breast cancer cells have a high predilection for skeletal homing, where they may either induce osteolytic bone destruction or enter a latency period in which they remain quiescent. Breast cancer cells produce and encounter autocrine and paracrine cytokine signals in the bone microenvironment, which can influence their behavior in multiple ways. For example, these signals can promote the survival and dormancy of bone-disseminated cancer cells or stimulate proliferation. The interleukin-6 (IL-6) cytokine family, defined by its use of the glycoprotein 130 (gp130) co-receptor, includes interleukin-11 (IL-11), leukemia inhibitory factor (LIF), oncostatin M (OSM), ciliary neurotrophic factor (CNTF), and cardiotrophin-1 (CT-1), among others. These cytokines are known to have overlapping pleiotropic functions in different cell types and are important for cross-talk between bone-resident cells. IL-6 cytokines have also been implicated in the progression and metastasis of breast, prostate, lung, and cervical cancer, highlighting the importance of these cytokines in the tumor–bone microenvironment. This review will describe the role of these cytokines in skeletal remodeling and cancer progression both within and outside of the bone microenvironment. -
Due to Interleukin-6 Type Cytokine Redundancy Only Glycoprotein 130 Receptor Blockade Efficiently Inhibits Myeloma Growth
Plasma Cell Disorders SUPPLEMENTARY APPENDIX Due to interleukin-6 type cytokine redundancy only glycoprotein 130 receptor blockade efficiently inhibits myeloma growth Renate Burger, 1 Andreas Günther, 1 Katja Klausz, 1 Matthias Staudinger, 1 Matthias Peipp, 1 Eva Maria Murga Penas, 2 Stefan Rose-John, 3 John Wijdenes 4 and Martin Gramatzki 1 1Division of Stem Cell Transplantation and Immunotherapy, Department of Internal Medicine II, Christian-Albrechts-University Kiel and University Medical Center Schleswig-Holstein, Kiel, Germany; 2Institute of Human Genetics, Christian-Albrechts-University Kiel and Uni - versity Medical Center Schleswig-Holstein, Kiel, Germany; 3Department of Biochemistry, Christian-Albrechts-University of Kiel, Medical Faculty, Germany and 4Gen-Probe/Diaclone SAS, Besançon, France ©2017 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol. 2016.145060 Received: February 25, 2016. Accepted: September 14, 2016. Pre-published: September 22, 2016. Correspondence: [email protected] SUPPLEMENTARY METHODS Cell lines and culture Cell lines INA-6, INA-6.Tu1 and B9 were cultivated in RPMI-1640 with GlutaMax™-I, 25 mM HEPES (Gibco®/Life Technologies GmbH, Darmstadt, Germany), 10% (v/v) heat-inactivated fetal bovine serum (FBS) (HyClone; Perbio Science, Erembodegen, Belgium), and antibiotics (R10+ medium) supplemented with 2.5 ng/ml recombinant huIL-6 (Gibco®/Life Technologies GmbH, Darmstadt, Germany). The cell lines are routinely confirmed to be negative for mycoplasma contamination (Venor™GeM Mycoplasma Detection Kit, Sigma-Aldrich, St. Louis, MO). Cytokines and other reagents Recombinant huIL-6 was purchased from Gibco®/Life Technologies (Darmstadt, Germany), huLIF was from Reliatech (Wolfenbüttel, Germany). Recombinant muIL-6 was obtained from Peprotech (Rocky Hill, NJ), and soluble muIL-6R was from R&D Systems (Minneapolis, MN). -
Characterization of Murine CD70, the Ligand of the TNF Receptor Family Member CD 27
UvA-DARE (Digital Academic Repository) Characterization of murine CD70, the ligand of the TNF receptor family member CD 27 Tesselaar, N.A.; Gravestein, L.A.; van Schijndel, G.; Borst, J.; van Lier, R.A.W. Publication date 1997 Published in The journal of immunology Link to publication Citation for published version (APA): Tesselaar, N. A., Gravestein, L. A., van Schijndel, G., Borst, J., & van Lier, R. A. W. (1997). Characterization of murine CD70, the ligand of the TNF receptor family member CD 27. The journal of immunology, 159, 4959-4965. General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. UvA-DARE is a service provided by the library of the University of Amsterdam (https://dare.uva.nl) Download date:30 Sep 2021 Characterization of Murine CD70, the Ligand of the TNF Receptor Family Member CD27' Kiki Tesselaar,* Loes A. -
Evolutionary Divergence and Functions of the Human Interleukin (IL) Gene Family Chad Brocker,1 David Thompson,2 Akiko Matsumoto,1 Daniel W
UPDATE ON GENE COMPLETIONS AND ANNOTATIONS Evolutionary divergence and functions of the human interleukin (IL) gene family Chad Brocker,1 David Thompson,2 Akiko Matsumoto,1 Daniel W. Nebert3* and Vasilis Vasiliou1 1Molecular Toxicology and Environmental Health Sciences Program, Department of Pharmaceutical Sciences, University of Colorado Denver, Aurora, CO 80045, USA 2Department of Clinical Pharmacy, University of Colorado Denver, Aurora, CO 80045, USA 3Department of Environmental Health and Center for Environmental Genetics (CEG), University of Cincinnati Medical Center, Cincinnati, OH 45267–0056, USA *Correspondence to: Tel: þ1 513 821 4664; Fax: þ1 513 558 0925; E-mail: [email protected]; [email protected] Date received (in revised form): 22nd September 2010 Abstract Cytokines play a very important role in nearly all aspects of inflammation and immunity. The term ‘interleukin’ (IL) has been used to describe a group of cytokines with complex immunomodulatory functions — including cell proliferation, maturation, migration and adhesion. These cytokines also play an important role in immune cell differentiation and activation. Determining the exact function of a particular cytokine is complicated by the influence of the producing cell type, the responding cell type and the phase of the immune response. ILs can also have pro- and anti-inflammatory effects, further complicating their characterisation. These molecules are under constant pressure to evolve due to continual competition between the host’s immune system and infecting organisms; as such, ILs have undergone significant evolution. This has resulted in little amino acid conservation between orthologous proteins, which further complicates the gene family organisation. Within the literature there are a number of overlapping nomenclature and classification systems derived from biological function, receptor-binding properties and originating cell type. -
Open Chen-Thesis Finalv5.Pdf
The Pennsylvania State University The Graduate School Department of Neural and Behavioral Sciences EPIGENETIC ANALYSIS OF IMMUNE ASSOCIATED SIGNALING MOLECULES DURING MOUSE RETINA DEVELOPMENT A Thesis in Anatomy by Chen Yang © 2013 Chen Yang Submitted in Partial Fulfillment of the Requirements for the Degree of Master of Science May 2013 The thesis of Chen Yang was reviewed and approved* by the following: Samuel Shao-Min Zhang Assistant Professor of Neural and Behavioral Sciences Thesis Advisor Colin J. Barnstable Department Head of Neural and Behavioral Sciences Professor of Neural and Behavioral Sciences Patricia J. McLaughlin Professor of Neural and Behavioral Sciences Director of Graduate Program in Anatomy *Signatures are on file in the Graduate School. ii ABSTRACT The retina is an immune-privileged organ. Many autoimmune diseases, such as AMD, glaucoma, and diabetic retinopathy, are caused by excessive inflammatory responses targeting self-tissue. The physiological functions of extracellular and intracellular signaling molecules of immune responses have been well characterized. The epigenetic aspects of these molecules in the retina, however, have not been well elucidated. In this study, we examined the expression of selected immune-related genes, and their transcriptional accessibility via epigenetic mapping, cluster analysis, and RT-PCR. Among these genes, interleukin receptor related genes and intracellular signaling molecules exhibit higher transcriptional accessibility. Epigenetic mapping of the toll-like receptor (TLR) family revealed that 3 out of 13 TLRs exhibit H3K4me2 accumulation during retina development, suggesting that TLR2, TLR3, and TLR9 are the only TLR members expressed in the retina. Most of the NF-κB signaling molecules exhibited transcriptional accessibility, implying their essential roles in inflammatory regulation during retina maturation.