A Novel CD4+ CTL Subtype Characterized by Chemotaxis and Inflammation Is Involved in the Pathogenesis of Graves’ Orbitopa
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Killer-Like Receptors and GPR56 Progressive Expression Defines Cytokine Production of Human CD4+ Memory T Cells
ARTICLE https://doi.org/10.1038/s41467-019-10018-1 OPEN Killer-like receptors and GPR56 progressive expression defines cytokine production of human CD4+ memory T cells Kim-Long Truong1,7, Stephan Schlickeiser1,2,7, Katrin Vogt1, David Boës1, Katarina Stanko1, Christine Appelt1, Mathias Streitz1, Gerald Grütz1,2, Nadja Stobutzki1, Christian Meisel1, Christina Iwert1, Stefan Tomiuk3, Julia K. Polansky2,4, Andreas Pascher5, Nina Babel2,6, Ulrik Stervbo 6, Igor Sauer 5, Undine Gerlach5 & Birgit Sawitzki1,2 1234567890():,; All memory T cells mount an accelerated response on antigen reencounter, but significant functional heterogeneity is present within the respective memory T-cell subsets as defined by CCR7 and CD45RA expression, thereby warranting further stratification. Here we show that several surface markers, including KLRB1, KLRG1, GPR56, and KLRF1, help define low, high, or exhausted cytokine producers within human peripheral and intrahepatic CD4+ memory T-cell populations. Highest simultaneous production of TNF and IFN-γ is observed in KLRB1+KLRG1+GPR56+ CD4 T cells. By contrast, KLRF1 expression is associated with T-cell exhaustion and reduced TNF/IFN-γ production. Lastly, TCRβ repertoire analysis and in vitro differentiation support a regulated, progressive expression for these markers during CD4+ memory T-cell differentiation. Our results thus help refine the classification of human memory T cells to provide insights on inflammatory disease progression and immunotherapy development. 1 Institute of Medical Immunology, Charité – Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, 13353 Berlin, Germany. 2 Berlin-Brandenburg Center for Regenerative Therapies (BCRT), Charité – Universitätsmedizin Berlin, 13353 Berlin, Germany. 3 Milteny Biotec GmbH, 51429 Bergisch Gladbach, Germany. -
Modulation of Endotoxin-Induced Monokine Release in Human Monocytes by Lipid a Partial Structures That Inhibit Binding of '25I-Lipopolysaccharide
INFECTION AND IMMUNITY, Dec. 1992, p. 5145-5152 Vol. 60, No. 12 0019-9567/92/125145-08$02.00/0 Copyright © 1992, American Society for Microbiology Modulation of Endotoxin-Induced Monokine Release in Human Monocytes by Lipid A Partial Structures That Inhibit Binding of '25I-Lipopolysaccharide ARTUR J. ULMER,`* WERNER FEIST,' HOLGER HEINE,' TERUO KIRIKAE,2 FUMIKO KIRIKAE,2 SHOICHI KUSUMOTO,3 TSUNEO KUSAMA,4 HELMUT BRADE,2 ULRICH SCHADE,2 ERNST T. RIETSCHEL,2 AND HANS-DIETER FLAD' Department ofImmunology and Cell Biology' and Department ofImmunochemistry and Biochemical Microbiology,2 Forschungsinstitut Borstel, D-2061 Borstel, Gennany, and Department of Chemistry, Osaka University, Osaka, 3 and Daiichi Pharmaceutical Co. Ltd., Tokyo,4 Japan Received 15 June 1992/Accepted 24 September 1992 We have previously shown that the synthetic tetraacyl precursor Ia (compound 406, LA-14-PP, or lipid IVa) was not able to induce the production of tumor necrosis factor, interleukin-1, and interleukin-6 in human monocytes but strongly antagonized lipopolysaccharide (LPS)-induced formation of these monokines. This inhibition was detectable at the level of mRNA production. To achieve a better understanding of molecular basis of this inhibition, we investigated whether lipid A precursor Ia (LA-14-PP), Escherichia coli-type lipid A (LA-15-PP), Chromobacterium violaceum-type lipid A (LA-22-PP), and synthetic lipid A partial structures and analogs (LA-23-PP, LA-24-PP, and PE-4) were able to influence the binding of 125I-LPS to human monocytes and compared this inhibitory activity with the agonistic and antagonistic action in the induction of monokines in human monocytes. -
Antibody-Dependent Cellular Cytotoxicity Riiia and Mediate Γ
Effector Memory αβ T Lymphocytes Can Express Fc γRIIIa and Mediate Antibody-Dependent Cellular Cytotoxicity This information is current as Béatrice Clémenceau, Régine Vivien, Mathilde Berthomé, of September 27, 2021. Nelly Robillard, Richard Garand, Géraldine Gallot, Solène Vollant and Henri Vié J Immunol 2008; 180:5327-5334; ; doi: 10.4049/jimmunol.180.8.5327 http://www.jimmunol.org/content/180/8/5327 Downloaded from References This article cites 43 articles, 21 of which you can access for free at: http://www.jimmunol.org/content/180/8/5327.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 September 27, 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 © 2008 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Effector Memory ␣ T Lymphocytes Can Express Fc␥RIIIa and Mediate Antibody-Dependent Cellular Cytotoxicity1 Be´atrice Cle´menceau,*† Re´gine Vivien,*† Mathilde Berthome´,*† Nelly Robillard,‡ Richard Garand,‡ Ge´raldine Gallot,*† Sole`ne Vollant,*† and Henri Vie´2*† Human memory T cells are comprised of distinct populations with different homing potential and effector functions: central memory T cells that mount recall responses to Ags in secondary lymphoid organs, and effector memory T cells that confer immediate protection in peripheral tissues. -
NK Cell Memory to Cytomegalovirus: Implications for Vaccine Development
Review NK Cell Memory to Cytomegalovirus: Implications for Vaccine Development Calum Forrest 1 , Ariane Gomes 1 , Matthew Reeves 1,* and Victoria Male 2,* 1 Institute of Immunity & Transplantation, UCL, Royal Free Campus, London NW3 2PF, UK; [email protected] (C.F.); [email protected] (A.G.) 2 Department of Metabolism, Digestion and Reproduction, Imperial College London, Chelsea and Westminster Campus, London SW10 9NH, UK * Correspondence: [email protected] (M.R.); [email protected] (V.M.) Received: 24 June 2020; Accepted: 15 July 2020; Published: 20 July 2020 Abstract: Natural killer (NK) cells are innate lymphoid cells that recognize and eliminate virally-infected and cancerous cells. Members of the innate immune system are not usually considered to mediate immune memory, but over the past decade evidence has emerged that NK cells can do this in several contexts. Of these, the best understood and most widely accepted is the response to cytomegaloviruses, with strong evidence for memory to murine cytomegalovirus (MCMV) and several lines of evidence suggesting that the same is likely to be true of human cytomegalovirus (HCMV). The importance of NK cells in the context of HCMV infection is underscored by the armory of NK immune evasion genes encoded by HCMV aimed at subverting the NK cell immune response. As such, ongoing studies that have utilized HCMV to investigate NK cell diversity and function have proven instructive. Here, we discuss our current understanding of NK cell memory to viral infection with a focus on the response to cytomegaloviruses. We will then discuss the implications that this will have for the development of a vaccine against HCMV with particular emphasis on how a strategy that can harness the innate immune system and NK cells could be crucial for the development of a vaccine against this high-priority pathogen. -
(TRAIL)-Mediated Apoptosis by Helicobacter Pylori in Immun
+ MODEL Journal of Microbiology, Immunology and Infection (2016) xx,1e6 Available online at www.sciencedirect.com ScienceDirect journal homepage: www.e-jmii.com REVIEW ARTICLE Modulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis by Helicobacter pylori in immune pathogenesis of gastric mucosal damage Hwei-Fang Tsai a,b, Ping-Ning Hsu c,d,* a Department of Internal Medicine, Taipei Medical University Shuang Ho Hospital, Taipei, Taiwan b Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan c Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan d Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan Received 1 March 2015; received in revised form 20 December 2015; accepted 17 January 2016 Available online --- KEYWORDS Abstract Helicobacter pylori infection is associated with chronic gastritis, peptic ulcer, apoptosis; gastric carcinoma, and gastric mucosa-associated lymphoid tissue lymphomas. Apoptosis chemokine; induced by microbial infections is implicated in the pathogenesis of H. pylori infection. FLIP; Enhanced gastric epithelial cell apoptosis during H. pylori infection was suggested to play Helicobacter pylori; an important role in the pathogenesis of chronic gastritis and gastric pathology. In addition TRAIL to directly triggering apoptosis, H. pylori induces sensitivity to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in gastric epithelial cells. Human gastric epithelial cells sensitized to H. pylori confer susceptibility to TRAIL-mediated apoptosis via modulation of death-receptor signaling. The induction of TRAIL sensitivity by H. pylori is dependent upon the activation of caspase-8 and its downstream pathway. H. pylori induces caspase-8 activation via enhanced assembly of the TRAIL death-inducing signaling complex through downregulation of cellular FLICE-inhibitory protein. -
Identification of Functional Thyroid Stimulating Hormone Receptor And
ANTICANCER RESEARCH 38 : 2793-2802 (2018) doi:10.21873/anticanres.12523 Identification of Functional Thyroid Stimulating Hormone Receptor and TSHR Gene Mutations in Hepatocellular Carcinoma YU-LIN SHIH 1,2 , YA-HUI HUANG 1, KWANG-HUEI LIN 1,3 , YU-DE CHU 1 and CHAU-TING YEH 1,2 1Liver Research Center, Chang Gung Memorial Hospital, Taoyuan, Taiwan, R.O.C.; 2Molecular Medicine Research Center, Chang Gung University, Taoyuan, Taiwan, R.O.C.; 3Department of Biochemistry, School of Medicine, Chang Gung University, Taoyuan, Taiwan, R.O.C. Abstract. Background/Aim: Extra-thyroid expression of viral hepatitis, alcohol abuse, non-alcoholic steatohepatitis, thyroid stimulating hormone (TSH) receptor (TSHR) has diabetes, aflatoxin, and cirrhosis (2). HCC can be treated by been reported in normal liver tissues, but never assessed in being completely removed/eradicated, with a liver hepatocellular carcinoma (HCC). Patients and Methods: transplantation, transcatheter arterial chemoembolization, or Paired cancerous and non-cancerous HCC tissues were with the use of targeted agents or systemic chemotherapy, analyzed with TSHR expression assays. TSHR functional depending on the clinical stage of the disease (3-5). Owing assessments and sequence analysis for the TSHR exon-10 to the asymptomatic nature of this disease, a great majority were performed. Results: TSHR overexpression was found in of patients (>50%) are diagnosed in the intermediate and 150/197 (76.1%) HCCs. Higher TSHR expression was advanced stages in Taiwan (6). associated with unfavorable postoperative outcomes. Thyroid hormone plays an essential role in the growth, Immunohistochemical analysis revealed predominantly maturation, differentiation and metabolism of normal cells nuclei/peri-nuclei localization of TSHR in cancerous tissues (7). -
Genitourinary Pathology (Including Renal Tumors)
LABORATORY INVESTIGATION THE BASIC AND TRANSLATIONAL PATHOLOGY RESEARCH JOURNAL LI VOLUME 99 | SUPPLEMENT 1 | MARCH 2019 2019 ABSTRACTS GENITOURINARY PATHOLOGY (INCLUDING RENAL TUMORS) (776-992) MARCH 16-21, 2019 PLATF OR M & 2 01 9 ABSTRACTS P OSTER PRESENTATI ONS EDUCATI ON C O M MITTEE Jason L. Hornick , C h air Ja mes R. Cook R h o n d a K. Y a nti s s, Chair, Abstract Revie w Board S ar a h M. Dr y and Assign ment Co m mittee Willi a m C. F a q ui n Laura W. La mps , Chair, C ME Subco m mittee C ar ol F. F ar v er St e v e n D. Billi n g s , Interactive Microscopy Subco m mittee Y uri F e d ori w Shree G. Shar ma , Infor matics Subco m mittee Meera R. Ha meed R aj a R. S e et h al a , Short Course Coordinator Mi c h ell e S. Hir s c h Il a n W ei nr e b , Subco m mittee for Unique Live Course Offerings Laksh mi Priya Kunju D a vi d B. K a mi n s k y ( Ex- Of ici o) A n n a M ari e M ulli g a n Aleodor ( Doru) Andea Ri s h P ai Zubair Baloch Vi nita Parkas h Olca Bast urk A nil P ar w a ni Gregory R. Bean , Pat h ol o gist-i n- Trai ni n g D e e p a P atil D a ni el J. -
And Α Mediated in Part by Enhanced IL-1 Formation in Spleen-Ost
1,25 (OH)2 Vitamin D3-Stimulated Osteoclast Formation in Spleen-Osteoblast Cocultures Is Mediated in Part by Enhanced IL-1α and Receptor Activator of NF- κB Ligand This information is current as Production in Osteoblasts of September 28, 2021. Sun-Kyeong Lee, Judy Kalinowski, Sandra Jastrzebski and Joseph A. Lorenzo J Immunol 2002; 169:2374-2380; ; doi: 10.4049/jimmunol.169.5.2374 Downloaded from http://www.jimmunol.org/content/169/5/2374 References This article cites 58 articles, 9 of which you can access for free at: http://www.jimmunol.org/ http://www.jimmunol.org/content/169/5/2374.full#ref-list-1 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 28, 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 © 2002 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology 1,25 (OH)2 Vitamin D3-Stimulated Osteoclast Formation in Spleen-Osteoblast Cocultures Is Mediated in Part by Enhanced IL-1␣ and Receptor Activator of NF-B Ligand Production in Osteoblasts1 Sun-Kyeong Lee,2 Judy Kalinowski, Sandra Jastrzebski, and Joseph A. -
Monoclonal Antibody to CD161 / KLRB1 - Purified
OriGene Technologies, Inc. OriGene Technologies GmbH 9620 Medical Center Drive, Ste 200 Schillerstr. 5 Rockville, MD 20850 32052 Herford UNITED STATES GERMANY Phone: +1-888-267-4436 Phone: +49-5221-34606-0 Fax: +1-301-340-8606 Fax: +49-5221-34606-11 [email protected] [email protected] SM1611PT Monoclonal Antibody to CD161 / KLRB1 - Purified Alternate names: C-type lectin domain family 5 member B, CLEC5B, HNKR-P1a, Killer cell lectin-like receptor subfamily B member 1, NKRP1A, Natural killer cell surface protein P1A Quantity: 25 µg Concentration: 1.0 mg/ml Background: Natural killer (NK) cells are lymphocytes that mediate cytotoxicity and secrete cytokines after immune stimulation. Several genes of the C-type lectin superfamily, including the rodent NKRP1 family of glycoproteins, are expressed by NK cells and may be involved in the regulation of NK cell function. The KLRB1 (CD161) protein contains an extracellular domain with several motifs characteristic of C type lectins, a transmembrane domain, and a cytoplasmic domain. The KLRB1 protein is classified as a type II membrane protein because it has an external C terminus. In mouse the NKRP1 family has three members, NKRP1A, B and C, whilst in human only one member has been identified. The human protein has received the designation CD161, and the mouse proteins have been referred to as CD161a, b and c. Engagement of CD161c has been reported to have activating function in NK cells, whilst engagement of CD161b is inhibitory. CD161 is expressed by almost all NK cells and with a small subset of CD3+ve T cells. -
Cytokine-Enhanced Cytolytic Activity of Exosomes from NK Cells
Cancer Gene Therapy https://doi.org/10.1038/s41417-021-00352-2 ARTICLE Cytokine-enhanced cytolytic activity of exosomes from NK Cells 1 1 2 3 2 3 Yutaka Enomoto ● Peng Li ● Lisa M. Jenkins ● Dimitrios Anastasakis ● Gaelyn C. Lyons ● Markus Hafner ● Warren J. Leonard 1 Received: 4 February 2021 / Revised: 9 May 2021 / Accepted: 18 May 2021 This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply 2021. This article is published with open access Abstract Natural killer (NK) cells play key roles in immune surveillance against tumors and viral infection. NK cells distinguish abnormal cells from healthy cells by cell–cell interaction with cell surface proteins and then attack target cells via multiple mechanisms. In addition, extracellular vesicles (EVs) derived from NK cells (NK-EVs), including exosomes, possess cytotoxic capacity against tumor cells, but their characteristics and regulation by cytokines remain unknown. Here, we report that EVs derived from human NK-92 cells stimulated with IL-15 + IL-21 show enhanced cytotoxic capacity against tumor cells. Major cytolytic granules, granzyme B and granzyme H, are enriched by IL-15 + IL-21 stimulation in NK-EVs; however, knockout experiments reveal those cytolytic granules are independent of enhanced cytotoxic capacity. To find out the key molecules, mass spectrometry analyses were 1234567890();,: 1234567890();,: performed with different cytokine conditions, no cytokine, IL-15, IL-21, or IL-15 + IL-21. We then found that CD226 (DNAM-1) on NK-EVs is enriched by IL-15 + IL-21 stimulation and that blocking antibodies against CD226 reduced the cytolytic activity of NK-EVs. -
Constitutive Activation of G Protein-Coupled Receptors and Diseases: Insights Into Mechanisms of Activation and Therapeutics
Pharmacology & Therapeutics 120 (2008) 129–148 Contents lists available at ScienceDirect Pharmacology & Therapeutics journal homepage: www.elsevier.com/locate/pharmthera Associate editor: S. Enna Constitutive activation of G protein-coupled receptors and diseases: Insights into mechanisms of activation and therapeutics Ya-Xiong Tao ⁎ Department of Anatomy, Physiology and Pharmacology, 212 Greene Hall, College of Veterinary Medicine, Auburn University, Auburn, AL 36849, USA article info abstract The existence of constitutive activity for G protein-coupled receptors (GPCRs) was first described in 1980s. In Keywords: 1991, the first naturally occurring constitutively active mutations in GPCRs that cause diseases were reported G protein-coupled receptor Disease in rhodopsin. Since then, numerous constitutively active mutations that cause human diseases were reported Constitutively active mutation in several additional receptors. More recently, loss of constitutive activity was postulated to also cause Inverse agonist diseases. Animal models expressing some of these mutants confirmed the roles of these mutations in the Mechanism of activation pathogenesis of the diseases. Detailed functional studies of these naturally occurring mutations, combined Transgenic model with homology modeling using rhodopsin crystal structure as the template, lead to important insights into the mechanism of activation in the absence of crystal structure of GPCRs in active state. Search for inverse Abbreviations: agonists on these receptors will be critical for correcting the diseases cause by activating mutations in GPCRs. ADRP, autosomal dominant retinitis pigmentosa Theoretically, these inverse agonists are better therapeutics than neutral antagonists in treating genetic AgRP, Agouti-related protein AR, adrenergic receptor diseases caused by constitutively activating mutations in GPCRs. CAM, constitutively active mutant © 2008 Elsevier Inc. -
REVIEW G-Protein-Coupled Receptors, Cholesterol and Palmitoylation: Facts
371 REVIEW G-protein-coupled receptors, cholesterol and palmitoylation: facts about fats Bice Chini and Marco Parenti1 Cellular and Molecular Pharmacology Section, CNR Institute of Neuroscience, Via Vanvitelli 32, 20129 Milan, Italy 1Department of Experimental Medicine, University of Milano-Bicocca, Monza, Italy (Correspondence should be addressed to B Chini; Email: [email protected]) Abstract G-protein-coupled receptors (GPCRs) are integral membrane proteins, hence it is not surprising that a number of their structural and functional features are modulated by both proteins and lipids. The impact of interacting proteins and lipids on the assembly and signalling of GPCRs has been extensively investigated over the last 20–30 years, and a further impetus has been given by the proposal that GPCRs and/or their immediate signalling partners (G proteins) can partition within plasma membrane domains, termed rafts and caveolae, enriched in glycosphingolipids and cholesterol. The high content of these specific lipids, in particular of cholesterol, in the vicinity of GPCR transmembranes can affect GPCR structure and/or function. In addition, most GPCRs are post-translationally modified with one or more palmitic acid(s), a 16-carbon saturated fatty acid, covalently bound to cysteine(s) localised in the carboxyl-terminal cytoplasmic tail. The insertion of palmitate into the cytoplasmic leaflet of the plasma membrane can create a fourth loop, thus profoundly affecting GPCR structure and hence the interactions with intracellular partner proteins. This review briefly highlights how lipids of the membrane and the receptor themselves can influence GPCR organisation and functioning. Journal of Molecular Endocrinology (2009) 42, 371–379 G-protein-coupled receptors–cholesterol of phospholipids.