BD Biosciences New RUO Reagents - November 2020
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The 'C3ar Antagonist' SB290157 Is a Partial C5ar2 Agonist
bioRxiv preprint doi: https://doi.org/10.1101/2020.08.01.232090; this version posted August 3, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. The ‘C3aR antagonist’ SB290157 is a partial C5aR2 agonist Xaria X. Li1, Vinod Kumar1, John D. Lee1, Trent M. Woodruff1* 1School of Biomedical Sciences, The University of Queensland, St Lucia, 4072 Australia. * Correspondence: Prof. Trent M. Woodruff School of Biomedical Sciences, The University of Queensland, St Lucia, 4072 Australia. Ph: +61 7 3365 2924; Fax: +61 7 3365 1766; E-mail: [email protected] Keywords: Complement C3a, C3aR, SB290157, C5aR1, C5aR2 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.08.01.232090; this version posted August 3, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Abbreviations used in this article: BRET, bioluminescence resonance energy transfer; BSA, bovine serum albumin; C3aR, C3a receptor C5aR1, C5a receptor 1; CHO-C3aR, Chinese hamster ovary cells stably expressing C3aR; CHO-C5aR1, Chinese hamster ovary cells stably expressing C5aR1; DMEM, Dulbecco's Modified Eagle's Medium; ERK1/2, extracellular signal-regulated kinase 1/2; FBS, foetal bovine serum; HEK293, human embryonic kidney 293 cells; HMDM, human monocyte-derived macrophage; i.p., intraperitoneal; i.v., intravenous; rhC5a, recombinant human C5a; RT, room temperature; S.E.M. -
Profound Treg Perturbations Correlate with COVID-19 Severity
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.11.416180; this version posted December 15, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Profound Treg perturbations correlate with COVID-19 severity Silvia Galván-Peña1*, Juliette Leon1,2*, Kaitavjeet Chowdhary1, Daniel A. Michelson1, Brinda Vijaykumar1, Liang Yang1, Angela Magnuson1, Zachary Manickas-Hill3,4, Alicja Piechocka- Trocha3,4, Daniel P. Worrall3,4, Kathryn E. Hall3,5, Musie Ghebremichael3,4, Bruce D. Walker3,4,6, Jonathan Z. Li3,7, Xu G. Yu3,4, MGH COVID-19 Collection & Processing Team, Diane Mathis1 and Christophe Benoist1,8,+ 1Department of Immunology, Harvard Medical School, Boston, MA, USA 2 INSERM UMR 1163, University of Paris, Imagine Institute, Paris, France 3Massachusetts Consortium on Pathogen Readiness, Boston, MA, USA 4Ragon Institute of MGH, MIT and Harvard, Cambridge, MA, USA 5Department of Medicine, Massachusetts General Hospital, Boston, MA, USA 6Howard Hughes Medical Institute, Center for the AIDS Programme of Research in South Africa. 7Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA 8Lead contact * Equal contribution +Address correspondence to: Christophe Benoist Department of Immunology Harvard Medical School 77 Avenue Louis Pasteur, Boston, MA 02115 e-mail: [email protected] Phone: (617) 432-7741 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.12.11.416180; this version posted December 15, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. -
Gene List HTG Edgeseq Immuno-Oncology Assay
Gene List HTG EdgeSeq Immuno-Oncology Assay Adhesion ADGRE5 CLEC4A CLEC7A IBSP ICAM4 ITGA5 ITGB1 L1CAM MBL2 SELE ALCAM CLEC4C DST ICAM1 ITGA1 ITGA6 ITGB2 LGALS1 MUC1 SVIL CDH1 CLEC5A EPCAM ICAM2 ITGA2 ITGAL ITGB3 LGALS3 NCAM1 THBS1 CDH5 CLEC6A FN1 ICAM3 ITGA4 ITGAM ITGB4 LGALS9 PVR THY1 Apoptosis APAF1 BCL2 BID CARD11 CASP10 CASP8 FADD NOD1 SSX1 TP53 TRAF3 BCL10 BCL2L1 BIRC5 CASP1 CASP3 DDX58 NLRP3 NOD2 TIMP1 TRAF2 TRAF6 B-Cell Function BLNK BTLA CD22 CD79A FAS FCER2 IKBKG PAX5 SLAMF1 SLAMF7 SPN BTK CD19 CD24 EBF4 FASLG IKBKB MS4A1 RAG1 SLAMF6 SPI1 Cell Cycle ABL1 ATF1 ATM BATF CCND1 CDK1 CDKN1B NCL RELA SSX1 TBX21 TP53 ABL2 ATF2 AXL BAX CCND3 CDKN1A EGR1 REL RELB TBK1 TIMP1 TTK Cell Signaling ADORA2A DUSP4 HES1 IGF2R LYN MAPK1 MUC1 NOTCH1 RIPK2 SMAD3 STAT5B AKT3 DUSP6 HES5 IKZF1 MAF MAPK11 MYC PIK3CD RNF4 SOCS1 STAT6 BCL6 ELK1 HEY1 IKZF2 MAP2K1 MAPK14 NFATC1 PIK3CG RORC SOCS3 SYK CEBPB EP300 HEY2 IKZF3 MAP2K2 MAPK3 NFATC3 POU2F2 RUNX1 SPINK5 TAL1 CIITA ETS1 HEYL JAK1 MAP2K4 MAPK8 NFATC4 PRKCD RUNX3 STAT1 TCF7 CREB1 FLT3 HMGB1 JAK2 MAP2K7 MAPKAPK2 NFKB1 PRKCE S100B STAT2 TYK2 CREB5 FOS HRAS JAK3 MAP3K1 MEF2C NFKB2 PTEN SEMA4D STAT3 CREBBP GATA3 IGF1R KIT MAP3K5 MTDH NFKBIA PYCARD SMAD2 STAT4 Chemokine CCL1 CCL16 CCL20 CCL25 CCL4 CCR2 CCR7 CX3CL1 CXCL12 CXCL3 CXCR1 CXCR6 CCL11 CCL17 CCL21 CCL26 CCL5 CCR3 CCR9 CX3CR1 CXCL13 CXCL5 CXCR2 MST1R CCL13 CCL18 CCL22 CCL27 CCL7 CCR4 CCRL2 CXCL1 CXCL14 CXCL6 CXCR3 PPBP CCL14 CCL19 CCL23 CCL28 CCL8 CCR5 CKLF CXCL10 CXCL16 CXCL8 CXCR4 XCL2 CCL15 CCL2 CCL24 CCL3 CCR1 CCR6 CMKLR1 CXCL11 CXCL2 CXCL9 CXCR5 -
The Expression and Regulation of Chemerin in the Epidermis
RESEARCH ARTICLE The Expression and Regulation of Chemerin in the Epidermis Magdalena Banas1, Aneta Zegar1, Mateusz Kwitniewski1, Katarzyna Zabieglo1, Joanna Marczynska1, Monika Kapinska-Mrowiecka2, Melissa LaJevic3,4, Brian A. Zabel4, Joanna Cichy1* 1 Department of Immunology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Kraków, Poland, 2 Department of Dermatology, Zeromski Hospital, Kraków, Poland, 3 Stanford University School of Medicine, Department of Pathology, Stanford, California, United States of America, 4 Palo Alto Veterans Institute for Research, VA Palo Alto Health Care System, Palo Alto, California, United States of America * [email protected] Abstract OPEN ACCESS Chemerin is a protein ligand for the G protein-coupled receptor CMKLR1 and also binds to two atypical heptahelical receptors, CCRL2 and GPR1. Chemerin is a leukocyte attractant, Citation: Banas M, Zegar A, Kwitniewski M, Zabieglo K, Marczynska J, Kapinska-Mrowiecka M, et al. adipokine, and antimicrobial protein. Although chemerin was initially identified as a highly (2015) The Expression and Regulation of Chemerin expressed gene in healthy skin keratinocytes that was downregulated during psoriasis, the in the Epidermis. PLoS ONE 10(2): e0117830. regulation of chemerin and its receptors in the skin by specific cytokines and microbial fac- doi:10.1371/journal.pone.0117830 tors remains unexplored. Here we show that chemerin, CMKLR1, CCRL2 and GPR1 are Academic Editor: Bernhard Ryffel, French National expressed in human and mouse epidermis, suggesting that this tissue may be both a Centre for Scientific Research, FRANCE source and target for chemerin mediated effects. In human skin cultures, chemerin is signifi- Received: October 1, 2014 cantly downregulated by IL-17 and IL-22, key cytokines implicated in psoriasis, whereas it is Accepted: December 31, 2014 upregulated by acute phase cytokines oncostatin M and IL-1β. -
Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association Between BMI and Adult-Onset Non- Atopic
Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association between BMI and Adult-Onset Non- Atopic Asthma Ayoung Jeong 1,2, Medea Imboden 1,2, Akram Ghantous 3, Alexei Novoloaca 3, Anne-Elie Carsin 4,5,6, Manolis Kogevinas 4,5,6, Christian Schindler 1,2, Gianfranco Lovison 7, Zdenko Herceg 3, Cyrille Cuenin 3, Roel Vermeulen 8, Deborah Jarvis 9, André F. S. Amaral 9, Florian Kronenberg 10, Paolo Vineis 11,12 and Nicole Probst-Hensch 1,2,* 1 Swiss Tropical and Public Health Institute, 4051 Basel, Switzerland; [email protected] (A.J.); [email protected] (M.I.); [email protected] (C.S.) 2 Department of Public Health, University of Basel, 4001 Basel, Switzerland 3 International Agency for Research on Cancer, 69372 Lyon, France; [email protected] (A.G.); [email protected] (A.N.); [email protected] (Z.H.); [email protected] (C.C.) 4 ISGlobal, Barcelona Institute for Global Health, 08003 Barcelona, Spain; [email protected] (A.-E.C.); [email protected] (M.K.) 5 Universitat Pompeu Fabra (UPF), 08002 Barcelona, Spain 6 CIBER Epidemiología y Salud Pública (CIBERESP), 08005 Barcelona, Spain 7 Department of Economics, Business and Statistics, University of Palermo, 90128 Palermo, Italy; [email protected] 8 Environmental Epidemiology Division, Utrecht University, Institute for Risk Assessment Sciences, 3584CM Utrecht, Netherlands; [email protected] 9 Population Health and Occupational Disease, National Heart and Lung Institute, Imperial College, SW3 6LR London, UK; [email protected] (D.J.); [email protected] (A.F.S.A.) 10 Division of Genetic Epidemiology, Medical University of Innsbruck, 6020 Innsbruck, Austria; [email protected] 11 MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, W2 1PG London, UK; [email protected] 12 Italian Institute for Genomic Medicine (IIGM), 10126 Turin, Italy * Correspondence: [email protected]; Tel.: +41-61-284-8378 Int. -
An Overview on G Protein-Coupled Receptor-Induced Signal Transduction in Acute Myeloid Leukemia
An overview on G protein-coupled receptor-induced signal transduction in Acute Myeloid Leukemia 1* 1,3 4,5,6 2* Frode Selheim , Elise Aasebø , Catalina Ribas and Anna M. Aragay 1The Proteomics Unit at the University of Bergen, Department of Biomedicine, University of Bergen, Jonas Lies vei 91, 5020 Bergen, Norway; 3 Department of Clinical Science, University of Bergen, Jonas Lies vei 87, 5021 Bergen, Norway; [email protected]. 2Departamento de Biologia Celular. Instituto de Biología Molecular de Barcelona (IBMB-CSIC), Spanish National Research Council (CSIC), Baldiri i Reixac, 15, 08028 Barcelona, Spain; [email protected]. 4Departamento de Biología Molecular and Centro de Biología Molecular “Severo Ochoa” (UAM-CSIC), 28049 Madrid, Spain; 5Instituto de Investigación Sanitaria La Princesa, 28006 Madrid, Spain; 6CIBER de Enfermedades Cardiovasculares, ISCIII (CIBERCV), 28029 Madrid, Spain, [email protected] * Corresponding authors: Frode Selheim Adr: Jonas Lies vei 91, 5020 Bergen, Norway Email: [email protected], Tel:+4755586091 Anna M. Aragay Adr: Baldiri i Reixac, 15, 08028 Barcelona. Spain. E-mail: [email protected]; Tel.: +934098671 1 Abstract Background: Acute myeloid leukemia (AML) is a genetically heterogeneous disease characterized by uncontrolled proliferation of precursor myeloid-lineage cells in the bone marrow. AML is also characterized with patients with poor long-term survival outcomes due to relapse. Many efforts have been made to understand the biological heterogeneity of AML and the challenges to develop new therapies are therefore enormous. G protein-coupled receptors (GPCRs) are a large attractive drug targeted family of transmembrane proteins, and aberrant GPCR expression and GPCR-mediated signaling have been implicated in leukemogenesis of AML. -
G Protein-Coupled Receptors
S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2015/16: G protein-coupled receptors. British Journal of Pharmacology (2015) 172, 5744–5869 THE CONCISE GUIDE TO PHARMACOLOGY 2015/16: G protein-coupled receptors Stephen PH Alexander1, Anthony P Davenport2, Eamonn Kelly3, Neil Marrion3, John A Peters4, Helen E Benson5, Elena Faccenda5, Adam J Pawson5, Joanna L Sharman5, Christopher Southan5, Jamie A Davies5 and CGTP Collaborators 1School of Biomedical Sciences, University of Nottingham Medical School, Nottingham, NG7 2UH, UK, 2Clinical Pharmacology Unit, University of Cambridge, Cambridge, CB2 0QQ, UK, 3School of Physiology and Pharmacology, University of Bristol, Bristol, BS8 1TD, UK, 4Neuroscience Division, Medical Education Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK, 5Centre for Integrative Physiology, University of Edinburgh, Edinburgh, EH8 9XD, UK Abstract The Concise Guide to PHARMACOLOGY 2015/16 provides concise overviews of the key properties of over 1750 human drug targets with their pharmacology, plus links to an open access knowledgebase of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. The full contents can be found at http://onlinelibrary.wiley.com/doi/ 10.1111/bph.13348/full. G protein-coupled receptors are one of the eight major pharmacological targets into which the Guide is divided, with the others being: ligand-gated ion channels, voltage-gated ion channels, other ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. -
Malaria Polyclonal B Cell Activator Activation of the Memory
Increased B Cell Survival and Preferential Activation of the Memory Compartment by a Malaria Polyclonal B Cell Activator This information is current as Daria Donati, Bobo Mok, Arnaud Chêne, Hong Xu, Mathula of October 2, 2021. Thangarajh, Rickard Glas, Qijun Chen, Mats Wahlgren and Maria Teresa Bejarano J Immunol 2006; 177:3035-3044; ; doi: 10.4049/jimmunol.177.5.3035 http://www.jimmunol.org/content/177/5/3035 Downloaded from References This article cites 35 articles, 15 of which you can access for free at: http://www.jimmunol.org/content/177/5/3035.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 2, 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 © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Increased B Cell Survival and Preferential Activation of the Memory Compartment by a Malaria Polyclonal B Cell Activator1 Daria Donati,2† Bobo Mok,* Arnaud Cheˆne,*† Hong Xu,† Mathula Thangarajh,‡ Rickard Glas,† Qijun Chen,§ Mats Wahlgren,* and Maria Teresa Bejarano*† Chronic malaria infection is characterized by polyclonal B cell activation, hyperglobulinemia, and elevated titers of autoantibod- ies. -
Program in Lupus Monocytes to Turn on a Migratory Dendritic Cell IFN
IFN Priming Is Necessary but Not Sufficient To Turn on a Migratory Dendritic Cell Program in Lupus Monocytes This information is current as Alicia Rodriguez-Pla, Pinakeen Patel, Holden T. Maecker, of September 28, 2021. Jose Rossello-Urgell, Nicole Baldwin, Lynda Bennett, Victoria Cantrell, Jeanine Baisch, Marilynn Punaro, Alisa Gotte, Lorien Nassi, Tracey Wright, Anna Karolina Palucka, Jacques Banchereau and Virginia Pascual J Immunol 2014; 192:5586-5598; Prepublished online 14 Downloaded from May 2014; doi: 10.4049/jimmunol.1301319 http://www.jimmunol.org/content/192/12/5586 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2014/05/14/jimmunol.130131 Material 9.DCSupplemental References This article cites 70 articles, 26 of which you can access for free at: http://www.jimmunol.org/content/192/12/5586.full#ref-list-1 Why The JI? Submit online. by guest on September 28, 2021 • 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: 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 © 2014 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. -
Novel Therapies for Eosinophilic Disorders
Novel Therapies for Eosinophilic Disorders Bruce S. Bochner, MD KEYWORDS Eosinophil Therapies Antibodies Targets Pharmacology Biomarkers KEY POINTS A sizable unmet need exists for new, safe, selective, and effective treatments for eosinophil-associated diseases, such as hypereosinophilic syndrome, eosinophilic gastrointestinal disorders, nasal polyposis, and severe asthma. An improved panel of biomarkers to help guide diagnosis, treatment, and assessment of disease activity is also needed. An impressive array of novel therapeutic agents, including small molecules and biologics, that directly or indirectly target eosinophils and eosinophilic inflammation are undergoing controlled clinical trials, with many already showing promising results. A large list of additional eosinophil-related potential therapeutic targets remains to be pursued, including cell surface structures, soluble proteins that influence eosinophil biology, and eosinophil-derived mediators that have the potential to contribute adversely to disease pathophysiology. INTRODUCTION Eosinophilic disorders, also referred to as eosinophil-associated diseases, consist of a range of infrequent conditions affecting virtually any body compartment and organ.1 The most commonly affected areas include the bone marrow, blood, mucosal sur- faces, and skin, often with immense disease- and treatment-related morbidity, Disclosure Statement: Dr Bochner’s research efforts are supported by grants AI072265, AI097073 and HL107151 from the National Institutes of Health. He has current or recent consul- ting or scientific advisory board arrangements with, or has received honoraria from, Sanofi-A- ventis, Pfizer, Svelte Medical Systems, Biogen Idec, TEVA, and Allakos, Inc. and owns stock in Allakos, Inc. and Glycomimetics, Inc. He receives publication-related royalty payments from Elsevier and UpToDate and is a coinventor on existing and pending Siglec-8-related patents and, thus, may be entitled to a share of future royalties received by Johns Hopkins University on the potential sales of such products. -
International Union of Basic and Clinical Pharmacology. LXXXVII
Supplemental Material can be found at: /content/suppl/2014/09/18/65.1.500.DC1.html 1521-0081/65/1/500–543$25.00 http://dx.doi.org/10.1124/pr.111.005223 PHARMACOLOGICAL REVIEWS Pharmacol Rev 65:500–543, January 2013 Copyright © 2013 by The American Society for Pharmacology and Experimental Therapeutics International Union of Basic and Clinical Pharmacology. LXXXVII. Complement Peptide C5a, C4a, and C3a Receptors Andreas Klos, Elisabeth Wende, Kathryn J. Wareham, and Peter N. Monk Department for Medical Microbiology, Medical School Hannover, Hannover, Germany (A.K., E.W.); and the Department of Infection and Immunity, University of Sheffield Medical School, Sheffield, United Kingdom (K.J.W., P.N.M.) Abstract. ....................................................................................502 I. Introduction. ..............................................................................503 A. Production of Complement Peptides......................................................503 B. Concentrations of Complement Peptides in Health and Disease. .........................503 C. C3a and C5a Generation outside the Complement Cascade ...............................504 D. Deactivation of Complement Peptides ....................................................505 II. The Role of Complement Peptides in Pathophysiology . .....................................505 A. Complement Peptides Are Important Biomarkers of Disease..............................505 B. Functions of the Complement Peptides beyond Innate Immunity .........................506 -
Techniques for Immune Function Analysis Application Handbook 1St Edition
Techniques for Immune Function Analysis Application Handbook 1st Edition BD Biosciences For additional information please access the Immune Function Homepage at www.bdbiosciences.com/immune_function For Research Use Only. Not for use in diagnostic or therapeutic procedures. Purchase does not include or carry any right to resell or transfer this product either as a stand-alone product or as a component of another product. Any use of this product other than the permitted use without the express written authorization of Becton Dickinson and Company is strictly prohibited. All applications are either tested in-house or reported in the literature. See Technical Data Sheets for details. BD, BD Logo and all other trademarks are the property of Becton, Dickinson and Company. ©2003 BD Table of Contents Preface . 4 Chapter 1: Immunofluorescent Staining of Cell Surface Molecules for Flow Cytometric Analysis . 9 Chapter 2: BD™ Cytometric Bead Array (CBA) Multiplexing Assays . 35 Chapter 3: BD™ DimerX MHC:Ig Proteins for the Analysis of Antigen-specific T Cells. 51 Chapter 4: Immunofluorescent Staining of Intracellular Molecules for Flow Cytometric Analysis . 61 Chapter 5: BD FastImmune™ Cytokine Flow Cytometry. 85 Chapter 6: BD™ ELISPOT Assays for Cells That Secrete Biological Response Modifiers . 109 Chapter 7: ELISA for Specifically Measuring the Levels of Cytokines, Chemokines, Inflammatory Mediators and their Receptors . 125 Chapter 8: BD OptEIA™ ELISA Sets and Kits for Quantitation of Analytes in Serum, Plasma, and Cell Culture Supernatants. 143 Chapter 9: BrdU Staining and Multiparameter Flow Cytometric Analysis of the Cell Cycle . 155 Chapter 10: Cell-based Assays for Biological Response Modifiers . 177 Chapter 11: BD RiboQuant™ Multi-Probe RNase Protection Assay System .