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The TNF and TNF Receptor Review Superfamilies: Integrating Mammalian Biology
Cell, Vol. 104, 487±501, February 23, 2001, Copyright 2001 by Cell Press The TNF and TNF Receptor Review Superfamilies: Integrating Mammalian Biology Richard M. Locksley,*²³k Nigel Killeen,²k The receptors and ligands in this superfamily have and Michael J. Lenardo§k unique structural attributes that couple them directly to *Department of Medicine signaling pathways for cell proliferation, survival, and ² Department of Microbiology and Immunology differentiation. Thus, they have assumed prominent ³ Howard Hughes Medical Institute roles in the generation of tissues and transient microen- University of California, San Francisco vironments. Most TNF/TNFR SFPs are expressed in the San Francisco, California 94143 immune system, where their rapid and potent signaling § Laboratory of Immunology capabilities are crucial in coordinating the proliferation National Institute of Allergy and Infectious Diseases and protective functions of pathogen-reactive cells. National Institutes of Health Here, we review the organization of the TNF/TNFR SF Bethesda, Maryland 20892 and how these proteins have been adapted for pro- cesses as seemingly disparate as host defense and or- ganogenesis. In interpreting this large and highly active Introduction area of research, we have focused on common themes that unite the actions of these genes in different tissues. Three decades ago, lymphotoxin (LT) and tumor necro- We also discuss the evolutionary success of this super- sis factor (TNF) were identified as products of lympho- familyÐsuccess that we infer from its expansion across cytes and macrophages that caused the lysis of certain the mammalian genome and from its many indispens- types of cells, especially tumor cells (Granger et al., able roles in mammalian biology. -
Human TNFRSF18 ELISA Kit (ARG81453)
Product datasheet [email protected] ARG81453 Package: 96 wells Human TNFRSF18 ELISA Kit Store at: 4°C Component Cat. No. Component Name Package Temp ARG81453-001 Antibody-coated 8 X 12 strips 4°C. Unused strips microplate should be sealed tightly in the air-tight pouch. ARG81453-002 Standard 2 X 10 ng/vial 4°C ARG81453-003 Standard/Sample 30 ml (Ready to use) 4°C diluent ARG81453-004 Antibody conjugate 1 vial (100 µl) 4°C concentrate (100X) ARG81453-005 Antibody diluent 12 ml (Ready to use) 4°C buffer ARG81453-006 HRP-Streptavidin 1 vial (100 µl) 4°C concentrate (100X) ARG81453-007 HRP-Streptavidin 12 ml (Ready to use) 4°C diluent buffer ARG81453-008 25X Wash buffer 20 ml 4°C ARG81453-009 TMB substrate 10 ml (Ready to use) 4°C (Protect from light) ARG81453-010 STOP solution 10 ml (Ready to use) 4°C ARG81453-011 Plate sealer 4 strips Room temperature Summary Product Description ARG81453 Human TNFRSF18 ELISA Kit is an Enzyme Immunoassay kit for the quantification of Human TNFRSF18 in serum, plasma (heparin, EDTA) and cell culture supernatants. Tested Reactivity Hu Tested Application ELISA Specificity There is no detectable cross-reactivity with other relevant proteins. Target Name TNFRSF18 Conjugation HRP Conjugation Note Substrate: TMB and read at 450 nm. Sensitivity 31.25 pg/ml Sample Type Serum, plasma (heparin, EDTA) and cell culture supernatants. Standard Range 62.5 - 4000 pg/ml Sample Volume 100 µl www.arigobio.com 1/3 Precision Intra-Assay CV: 6.3% Inter-Assay CV: 7.0% Alternate Names Tumor necrosis factor receptor superfamily member 18; AITR; CD357; CD antigen CD357; Activation- inducible TNFR family receptor; GITR-D; GITR; Glucocorticoid-induced TNFR-related protein Application Instructions Assay Time ~ 5 hours Properties Form 96 well Storage instruction Store the kit at 2-8°C. -
TNFRSF18 (Human) ELISA Kit
TNFRSF18 (Human) ELISA Kit Catalog Number KA1720 96 assays Version: 01 Intended for research use only www.abnova.com I. INTRODUCTION GITR (glucocorticoid induced tumor necrosis factor receptor family related gene) is a type-1 transmembrane protein of 228 amino acids belonging to the TNF and NGF receptor family of proteins. GITR is expressed in normal T-lymphocytes from thymus, spleen. Constitutive expression of a transfected GITR gene induces resistance to apoptosis induced by anti CD3 monoclonal antibodies. The human homolog of GITR is expressed in lymph node and peripheral blood leukocytes. Its expression is up-regulated in human peripheral mononuclear cells mainly after stimulation with antibodies against CD3 and CD28. TNFRSF18 (Human) ELISA Kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of human GITR in cell lysate and tissue lysate. This assay employs an antibody specific for human GITR coated on a 96-well plate. Standards and samples are pipetted into the wells and GITR present in a sample is bound to the wells by the immobilized antibody. The wells are washed and biotinylated anti-human GITR antibody is added. After washing away unbound biotinylated antibody, HRP-conjugated streptavidin is pipetted to the wells. The wells are again washed, a TMB substrate solution is added to the wells and color develops in proportion to the amount of GITR bound. The Stop Solution changes the color from blue to yellow, and the intensity of the color is measured at 450 nm. II. REAGENTS 1. GITR Microplate (Item A): 96 wells (12 strips x 8 wells) coated with anti-human GITR. -
Diverse Functional Autoantibodies in Patients with COVID-19
medRxiv preprint doi: https://doi.org/10.1101/2020.12.10.20247205; this version posted December 11, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . Diverse Functional Autoantibodies in Patients with COVID-19 Eric Y. Wang1,*, Tianyang Mao1,*, Jon Klein1,*, Yile Dai1,*, John D. Huck1, Feimei Liu1, Neil S. Zheng1, Ting Zhou1, Benjamin Israelow1, Patrick Wong1, Carolina Lucas1, Julio Silva1, Ji Eun Oh1, Eric Song1, Emily S. Perotti1, Suzanne Fischer1, Melissa Campbell5, John B. Fournier5, Anne L. Wyllie3, Chantal B. F. Vogels3, Isabel M. Ott3, Chaney C. Kalinich3, Mary E. Petrone3, Anne E. Watkins3, Yale IMPACT Team¶, Charles Dela Cruz4, Shelli F. Farhadian5, Wade L. Schulz6,7, Nathan D. Grubaugh3, Albert I. Ko3,5, Akiko Iwasaki1,3,8,#, Aaron M. Ring1,2,# 1 Department of Immunobiology, Yale School of Medicine, New Haven, CT, USA 2 Department of Pharmacology, Yale School of Medicine, New Haven, CT, USA 3 Department of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT, USA 4 Department of Medicine, Section of Pulmonary and Critical Care Medicine, Yale School of Medicine, New Haven, CT, USA 5 Department of Internal Medicine (Infectious Diseases), Yale School of Medicine, New Haven, CT, USA 6 Department of Laboratory Medicine, Yale School of Medicine, New Haven, CT, USA 7 Center for Outcomes Research and Evaluation, Yale-New Haven Hospital, New Haven, CT, USA 8 Howard Hughes Medical Institute, Chevy Chase, MD, USA * These authors contributed equally to this work ¶ A list of authors and their affiliations appears at the end of the paper # Correspondence: [email protected] (A.M.R.); [email protected] (A.I.) 1 NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. -
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. -
Prevalent Homozygous Deletions of Type I Interferon and Defensin Genes in Human Cancers Associate with Immunotherapy Resistance
Author Manuscript Published OnlineFirst on April 4, 2018; DOI: 10.1158/1078-0432.CCR-17-3008 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Prevalent Homozygous Deletions of Type I Interferon and Defensin Genes in Human Cancers Associate with Immunotherapy Resistance Zhenqing Ye1; Haidong Dong2,3; Ying Li1; Tao Ma1,4; Haojie Huang4; Hon-Sing Leong4; Jeanette Eckel-Passow1; Jean-Pierre A. Kocher1; Han Liang5; LiguoWang1,4,* 1Division of Biomedical Statistics and Informatics, Department of Health Sciences, Mayo Clinic, Rochester, Minnesota 55905, United States of America 2Department of Immunology, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, United States of America 3Department of Urology, Mayo Clinic, Rochester, Minnesota 55905, United States of America 4Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905, United States of America 5Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, United States of America Running title: Pervasive Deletion of Interferon/Defensin in Human Cancers Keywords: Homozygous deletion, Type-I interferon, Defensin, immunotherapy resistance, cancer * Correspondence to: Liguo Wang, Ph.D. Associate Professor Division of Biomedical Statistics and Informatics, Mayo Clinic 200 1st St SW Rochester, MN 55905, USA Phone: +1-507-284-8728 Fax: +1-507-284-0745 Email: [email protected] The authors declare no potential conflicts of interest. 1 Downloaded from clincancerres.aacrjournals.org on September 29, 2021. © 2018 American Association for Cancer Research. Author Manuscript Published OnlineFirst on April 4, 2018; DOI: 10.1158/1078-0432.CCR-17-3008 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. -
Specialized Interferon Ligand Action in COVID19
medRxiv preprint doi: https://doi.org/10.1101/2021.07.29.21261325; this version posted August 1, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license . Specialized interferon ligand action in COVID19 Matthew D. Galbraith1,2, Kohl T. Kinning1, Kelly D. Sullivan1,3, Paula Araya1, Keith P. Smith1, Ross E. Granrath1, Jessica R. Shaw1, Ryan Baxter4, Kimberly R. Jordan4, Seth Russell5, Monika Dzieciatkowska6, Julie A. Reisz6, Fabia Gamboni6, Francesca CenDali6, Tusharkanti Ghosh7, AnDrew A. Monte8, Tellen D. Bennett9, Kirk C. Hansen6, Elena W.Y. Hsieh4,10, Angelo D’AlessanDro6, and Joaquin M. Espinosa1,2* Affiliations: 1Linda Crnic Institute for Down SynDrome, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 2Department of Pharmacology, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 3Department of PeDiatrics, Section of Developmental Biology, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 4Department of Immunology anD Microbiology, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 5Data Science to Patient Value, University of Colorado Anschutz Medical Campus; Aurora, CO, USA. 6Department of Biochemistry anD Molecular Genetics, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 7Department of Biostatistics anD Informatics, ColoraDo School of Public Health; Aurora, CO, USA. 8Department of Emergency MeDicine, University of ColoraDo Anschutz MeDical Campus; Aurora, CO, USA. 9Department of PeDiatrics, Sections of Informatics anD Data Science anD Critical Care MeDicine, University of ColoraDo Anschutz Medical Campus; Aurora, CO, USA. -
Human GITR/TNFRSF18 Alexa Fluor® 700-Conjugated Antibody
Human GITR/TNFRSF18 Alexa Fluor® 700-conjugated Antibody Monoclonal Mouse IgG1 Clone # 110416 Catalog Number: FAB689N 100 Tests, 25 Tests DESCRIPTION Species Reactivity Human Specificity Detects human GITR in direct ELISAs and Western blots. Does not crossreact with recombinant human (rh) 41BB, recombinant mouse (rm) 41BB, rhCD27, rmCD27, rhCD30, rmCD30, rhCD40, rmCD40, rhDR3, rhDR6, rhEDAR, rmEDAR, rhFas, rmFAS, rmGITR, rhHVEM, rhLymphotoxin Rβ, rmLymphotoxin Rβ, rhNGF R, rhOPG, rmOPG, rhRANK, rmRANK, rhTAJ, rhTNF RI, rmTNF RI, rhTNF RII, or rmTNF RII. Source Monoclonal Mouse IgG1 Clone # 110416 Purification Protein A or G purified from hybridoma culture supernatant Immunogen Mouse myeloma cell line NS0derived recombinant human GITR/TNFRSF18 Gln26Glu161 (Thr43Ala) Accession # Q9Y5U5 Conjugate Alexa Fluor 700 Excitation Wavelength: 675700 nm Emission Wavelength: 723 nm Formulation Supplied in a saline solution containing BSA and Sodium Azide. See Certificate of Analysis for details. *Contains <0.1% Sodium Azide, which is not hazardous at this concentration according to GHS classifications. Refer to the Safety Data Sheet (SDS) for additional information and handling instructions. APPLICATIONS Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website. Recommended Sample Concentration Flow Cytometry 5 µL/106 cells See Below DATA Flow Cytometry Detection of GITR/TNFRSF18 in Human PBMCs by Flow Cytometry. Human peripheral blood mononuclear cells (PBMCs) treated with 5 μg/mL PHA for 5 days were stained with Mouse Anti Human CD4 PEconjugated Monoclonal Antibody (Catalog # FAB3791P) and either (A) Mouse AntiHuman GITR/TNFRSF18 Alexa Fluor® 700conjugated Monoclonal Antibody (Catalog # FAB689N) or (B) Mouse IgG1 Alexa Fluor 700 Isotype Control (Catalog # IC002N). -
KRAS Mutations Are Negatively Correlated with Immunity in Colon Cancer
www.aging-us.com AGING 2021, Vol. 13, No. 1 Research Paper KRAS mutations are negatively correlated with immunity in colon cancer Xiaorui Fu1,2,*, Xinyi Wang1,2,*, Jinzhong Duanmu1, Taiyuan Li1, Qunguang Jiang1 1Department of Gastrointestinal Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People's Republic of China 2Queen Mary College, Medical Department, Nanchang University, Nanchang, Jiangxi, People's Republic of China *Equal contribution Correspondence to: Qunguang Jiang; email: [email protected] Keywords: KRAS mutations, immunity, colon cancer, tumor-infiltrating immune cells, inflammation Received: March 27, 2020 Accepted: October 8, 2020 Published: November 26, 2020 Copyright: © 2020 Fu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT The heterogeneity of colon cancer tumors suggests that therapeutics targeting specific molecules may be effective in only a few patients. It is therefore necessary to explore gene mutations in colon cancer. In this study, we obtained colon cancer samples from The Cancer Genome Atlas, and the International Cancer Genome Consortium. We evaluated the landscape of somatic mutations in colon cancer and found that KRAS mutations, particularly rs121913529, were frequent and had prognostic value. Using ESTIMATE analysis, we observed that the KRAS-mutated group had higher tumor purity, lower immune score, and lower stromal score than the wild- type group. Through single-sample Gene Set Enrichment Analysis and Gene Set Enrichment Analysis, we found that KRAS mutations negatively correlated with enrichment levels of tumor infiltrating lymphocytes, inflammation, and cytolytic activities. -
Interferonsource.Com What's Inside New Products Research Tools Protocols & Tips Product Citations What's Your IFN-Α
Interferon Matters A quarterly newsletter by PBL InterferonSource interferonsource.com May 2007, Issue 2 u What’s Inside What’s Your IFN-a Type? New Products Are all Type I IFNs created equal? Of Mice and Men page 4 & 5 Type I Interferons were the first cytokines to be The biological significance of the expression of discovered. They are a family of homologous cytokines so many different IFN-a subtypes has yet to be Rhesus/Cynomolgus originally identified for their antiviral activity but have determined. However, reports suggest that they show IFN-a2 Subtype also been shown to have both anti-proliferative and quantitatively distinct anti-viral, anti-proliferative, immunomodulatory activities. In humans and mice and killer cell-stimulatory activities. It is therefore Mouse IFN-a4 Subtype they are encoded by an intronless multigene family of importance for researchers to characterize and clustered on human chromosome 9 and murine study these IFN-a subtypes and their possible post- chromosome 4 respectively. translational modifications. Research Tools Also in both species there are multiple Interferon- The common models for IFN-a subtypes study are page 6 & 7 Alpha (IFN-a) genes and one Interferon-Beta (IFN-b) human and mouse. In 1998, Lawson et al showed that Human IFN-a gene. Other Type I Interferon genes described include there are in vivo differences in the antiviral activity of the Interferon-Omega (IFN-w) gene, murine limitin the mouse IFN-a subtypes.1 Using an experimental Multi-Subtype ELISA Kit gene, as well as the human/murine Interferon-Epilson, mouse model of IFN transgene expression in vivo, TM Interferon-Kappa, and Interferon-Tau (IFN-e, IFN-k, and the authors showed that mouse IFN-a1 has a greater iLite Human IFN-a Kit IFN-t). -
Variation in the Type I Interferon Gene Cluster on 9P21 Influences Susceptibility to Asthma and Atopy
Genes and Immunity (2006) 7, 169–178 & 2006 Nature Publishing Group All rights reserved 1466-4879/06 $30.00 www.nature.com/gene ORIGINAL ARTICLE Variation in the type I interferon gene cluster on 9p21 influences susceptibility to asthma and atopy A Chan1,2, DL Newman1,3, AM Shon, DH Schneider, S Kuldanek and C Ober Department of Human Genetics, The University of Chicago, Chicago, IL, USA A genome-wide screen for asthma and atopy susceptibility alleles conducted in the Hutterites, a founder population of European descent, reported evidence of linkage with a short tandem repeat polymorphism (STRP) within the type I interferon (IFN) gene cluster on chromosome 9p21. The goal of this study was to identify variation within the IFN gene cluster that influences susceptibility to asthma and atopic phenotypes. We screened approximately 25 kb of sequence, including the flanking sequence of all 15 functional genes and the single coding exon in 12, in Hutterites representing different IFNA-STRP genotypes. We identified 78 polymorphisms, and genotyped 40 of these (in 14 genes) in a large Hutterite pedigree. Modest associations (0.003oPo0.05) with asthma, bronchial hyper-responsiveness (BHR), and atopy were observed with individual variants or genes, spanning the entire 400 kb region. However, pairwise combinations of haplotypes between genes showed highly significant associations with different phenotypes (Po10À5) that were localized to specific pairs of genes or regions of this cluster. These results suggest that variation in multiple genes in the type I IFN cluster on 9p22 contribute to asthma and atopy susceptibility, and that not all genes contribute equally to all phenotypes. -
Defining Molecular Adjuvant Effects on Human B Cell Subsets
DEFINING MOLECULAR ADJUVANT EFFECTS ON HUMAN B CELL SUBSETS A DISSERTATION SUBMITTED TO THE GRADUATE DIVISION OF THE UNIVERSITY OF HAWAIʻI AT MĀNOA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY IN BIOMEDICAL SCIENCES (TROPICAL MEDICINE) August 2019 By Jourdan Posner Dissertation Committee: Sandra P. Chang, Chairperson George Hui Saguna Verma William Gosnell Alan Katz ACKNOWLEDGMENTS First and foremost, I would like to express my gratitude to my PhD advisor and mentor, Dr. Sandra Chang. Her passion for science, scientific rigor, and inquisitive nature have been an inspiration to me. I am very grateful for her continuous support and mentorship. I would also like to thank my committee members, Dr. George Hui, Dr. Saguna Verma, Dr. William Gosnell, and Dr. Alan Katz, for their advice and support on this dissertation work. To my parasitology “dads”, Dr. Kenton Kramer and Dr. William Gosnell, I am forever grateful for all of the opportunities you’ve given to me. Your mentorship has guided me through the doctoral process and helped me to maintain “homeostasis”. Last, but not least, I’d like to thank my parents and brother who have been so supportive throughout my entire graduate career. I greatly appreciate all of the encouraging words and for always believing in me. And to my future husband, Ian, I could not have completed this dissertation work without your endless support. You are my rock. ii ABSTRACT Recent advances in vaccine development include the incorporation of novel adjuvants to increase vaccine immunogenicity and efficacy. Pattern recognition receptor (PRR) ligands are of particular interest as vaccine adjuvants.