The Immunological Synapse and CD28-CD80 Interactions Shannon K
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Costimulation of T-Cell Activation and Virus Production by B7 Antigen on Activated CD4+ T Cells from Human Immunodeficiency Virus Type 1-Infected Donors OMAR K
Proc. Natl. Acad. Sci. USA Vol. 90, pp. 11094-11098, December 1993 Immunology Costimulation of T-cell activation and virus production by B7 antigen on activated CD4+ T cells from human immunodeficiency virus type 1-infected donors OMAR K. HAFFAR, MOLLY D. SMITHGALL, JEFFREY BRADSHAW, BILL BRADY, NITIN K. DAMLE*, AND PETER S. LINSLEY Bristol-Myers Squibb Pharmaceutical Research Institute, Seattle, WA 98121 Communicated by Leon E. Rosenberg, August 3, 1993 (receivedfor review April 29, 1993) ABSTRACT Infection with the human immunodeficiency sequence (CTLA-4) (34), a protein structurally related to virus type 1 (HIV-1) requires T-cefl activation. Recent studies CD28 but only expressed on T cells after activation (12). have shown that interactions of the T-lymphocyte receptors CTLA-4 acts cooperatively with CD28 to bind B7 and deliver CD28 and CTLA-4 with their counter receptor, B7, on antigen- T-cell costimulatory signals (13). presenting cells are required for optimal T-cell activation. Here Because of the importance of the CD28/CTLA-4 and B7 we show that HIV-1 infection is associated with decreased interactions in immune responses, it is likely that these expression of CD28 and increased expression of B7 on CD4+ interactions are also important during HIV-1 infection. Stud- T-cell lines generated from seropositive donors by afloantigen ies with anti-CD28 monoclonal antibodies (mAbs) suggested stimulation. Loss of CD28 expression was not seen on CD4+ a role for CD28 in up-regulating HIV-1 long terminal repeat- T-ceU lines from seronegative donors, but up-regulation of B7 driven transcription of a reporter gene in leukemic cell lines expression was observed upon more prolonged culture. -
Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse
Welcome to More Choice CD Marker Handbook For more information, please visit: Human bdbiosciences.com/eu/go/humancdmarkers Mouse bdbiosciences.com/eu/go/mousecdmarkers Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse CD3 CD3 CD (cluster of differentiation) molecules are cell surface markers T Cell CD4 CD4 useful for the identification and characterization of leukocytes. The CD CD8 CD8 nomenclature was developed and is maintained through the HLDA (Human Leukocyte Differentiation Antigens) workshop started in 1982. CD45R/B220 CD19 CD19 The goal is to provide standardization of monoclonal antibodies to B Cell CD20 CD22 (B cell activation marker) human antigens across laboratories. To characterize or “workshop” the antibodies, multiple laboratories carry out blind analyses of antibodies. These results independently validate antibody specificity. CD11c CD11c Dendritic Cell CD123 CD123 While the CD nomenclature has been developed for use with human antigens, it is applied to corresponding mouse antigens as well as antigens from other species. However, the mouse and other species NK Cell CD56 CD335 (NKp46) antibodies are not tested by HLDA. Human CD markers were reviewed by the HLDA. New CD markers Stem Cell/ CD34 CD34 were established at the HLDA9 meeting held in Barcelona in 2010. For Precursor hematopoetic stem cell only hematopoetic stem cell only additional information and CD markers please visit www.hcdm.org. Macrophage/ CD14 CD11b/ Mac-1 Monocyte CD33 Ly-71 (F4/80) CD66b Granulocyte CD66b Gr-1/Ly6G Ly6C CD41 CD41 CD61 (Integrin b3) CD61 Platelet CD9 CD62 CD62P (activated platelets) CD235a CD235a Erythrocyte Ter-119 CD146 MECA-32 CD106 CD146 Endothelial Cell CD31 CD62E (activated endothelial cells) Epithelial Cell CD236 CD326 (EPCAM1) For Research Use Only. -
T-Cell Antigen CD28 Mediates Adhesion with B Cells by Interacting with Activation Antigen B7/BB-1 PETER S
Proc. Nati. Acad. Sci. USA Vol. 87, pp. 5031-5035, July 1990 Immunology T-cell antigen CD28 mediates adhesion with B cells by interacting with activation antigen B7/BB-1 PETER S. LINSLEY*, EDWARD A. CLARKt, AND JEFFREY A. LEDBETTER* *Oncogen, 3005 First Avenue, Seattle, WA 98121; and tDepartment of Microbiology, University of Washington, Seattle, WA 98195 Communicated by Seymour J. Klebanoff, March 30, 1990 ABSTRACT Studies using monoclonal antibodies (mAbs) intercellular adhesion mediated by major histocompatibility have implicated the homodimeric glycoprotein CD28 as an complex (MHC) class I (13) and class II (14) molecules with important regulator of human T-cell activation, in part by the CD8 and CD4 accessory molecules, respectively. We posttranscriptional control ofcytokine mRNA levels. Although have expressed the CD28 antigen to high levels in Chinese the CD28 antigen has functional and structural characteristics hamster ovary (CHO) cells and have used these transfected of a receptor, a natural ligand for this molecule has not been cells to develop a CD28-mediated cell adhesion assay. By identified. Here we show that the CD28 antigen, expressed in using this assay as a screening method, we have demon- Chinese hamster ovary (CHO) cells, mediated specific inter- strated an interaction between CD28 and a natural ligand cellular adhesion with human lymphoblastoid and leukemic expressed on activated B lymphocytes, the B7/BB-1 antigen. B-cell lines and with activated primary murine B cells. CD28- mediated adhesion was not, dependant upon divalent cations. Several mAbs were identified that inhibited CD28-mediated MATERIALS AND METHODS adhesion, including mAb BB-1 against the B-cell activation mAbs. -
Inhibition of Midkine Alleviates Experimental Autoimmune Encephalomyelitis Through the Expansion of Regulatory T Cell Population
Inhibition of midkine alleviates experimental autoimmune encephalomyelitis through the expansion of regulatory T cell population Jinyan Wang*, Hideyuki Takeuchi*†, Yoshifumi Sonobe*, Shijie Jin*, Tetsuya Mizuno*, Shin Miyakawa‡, Masatoshi Fujiwara‡, Yoshikazu Nakamura§¶, Takuma Katoʈ, Hisako Muramatsu**, Takashi Muramatsu**††, and Akio Suzumura*† *Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan; ‡RIBOMIC, Inc., 3-15-5-601 Shirokanedai, Minato-ku, Tokyo 108-0071, Japan; §Department of Basic Medical Sciences, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan; ¶Core Research Evolutional Science and Technology, Japan Science and Technology Agency, Toyonaka, Osaka 560-8531, Japan; ʈDepartment of Bioregulation, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan; **Department of Biochemistry, Nagoya University Graduate School of Medicine, Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan; and ††Department of Health Science, Faculty of Psychological and Physical Sciences, Aichi Gakuin University, Nisshin, Aichi 470-0195, Japan Edited by Ethan Shevach, National Institutes of Health, Bethesda, MD, and accepted by the Editorial Board January 20, 2008 (received for review October 12, 2007) CD4؉CD25؉ regulatory T (Treg) cells are crucial mediators of nity, and abnormalities in Treg cell function may contribute to the autoimmune tolerance. The factors that regulate Treg cells, how- development of -
Immunomodulation and Generation of Tolerogenic Dendritic Cells by Probiotic Bacteria in Patients with Inflammatory Bowel Disease
International Journal of Molecular Sciences Article Immunomodulation and Generation of Tolerogenic Dendritic Cells by Probiotic Bacteria in Patients with Inflammatory Bowel Disease 1, 2, 1 Shaghayegh Baradaran Ghavami y, Abbas Yadegar y , Hamid Asadzadeh Aghdaei , Dario Sorrentino 3,4,*, Maryam Farmani 1 , Adil Shamim Mir 5, Masoumeh Azimirad 2 , Hedieh Balaii 6, Shabnam Shahrokh 6 and Mohammad Reza Zali 6 1 Basic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran 1985717413, Iran; [email protected] (S.B.G.); [email protected] (H.A.A.); [email protected] (M.F.) 2 Foodborne and Waterborne Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran 1985717413, Iran; [email protected] (A.Y.); [email protected] (M.A.) 3 IBD Center, Division of Gastroenterology, Virginia Tech Carilion School of Medicine, Roanoke, VA 24016, USA 4 Department of Clinical and Experimental Medical Sciences, University of Udine School of Medicine, 33100 Udine, Italy 5 Department of Internal Medicine, Roanoke Memorial Hospital, Carilion Clinic, VA 24014, USA; [email protected] 6 Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran 1985717413, Iran; [email protected] (H.B.); [email protected] (S.S.); [email protected] (M.R.Z.) * Correspondence: [email protected] These authors equally contributed to this study. y Received: 7 August 2020; Accepted: 27 August 2020; Published: 29 August 2020 Abstract: In inflammatory bowel diseases (IBD), the therapeutic benefit and mucosal healing from specific probiotics may relate to the modulation of dendritic cells (DCs). -
Galectin-4 Interaction with CD14 Triggers the Differentiation of Monocytes Into Macrophage-Like Cells Via the MAPK Signaling Pathway
Immune Netw. 2019 Jun;19(3):e17 https://doi.org/10.4110/in.2019.19.e17 pISSN 1598-2629·eISSN 2092-6685 Original Article Galectin-4 Interaction with CD14 Triggers the Differentiation of Monocytes into Macrophage-like Cells via the MAPK Signaling Pathway So-Hee Hong 1,2,3,4,5, Jun-Seop Shin 1,2,3,5, Hyunwoo Chung 1,2,4,5, Chung-Gyu Park 1,2,3,4,5,* 1Xenotransplantation Research Center, Seoul National University College of Medicine, Seoul 03080, Korea 2Institute of Endemic Diseases, Seoul National University College of Medicine, Seoul 03080, Korea 3Cancer Research Institute, Seoul National University College of Medicine, Seoul 03080, Korea 4Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea 5Department of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Korea Received: Jan 28, 2019 ABSTRACT Revised: May 13, 2019 Accepted: May 19, 2019 Galectin-4 (Gal-4) is a β-galactoside-binding protein mostly expressed in the gastrointestinal *Correspondence to tract of animals. Although intensive functional studies have been done for other galectin Chung-Gyu Park isoforms, the immunoregulatory function of Gal-4 still remains ambiguous. Here, we Department of Microbiology and Immunology, Seoul National University College of Medicine, demonstrated that Gal-4 could bind to CD14 on monocytes and induce their differentiation 103 Daehak-ro, Jongno-gu, Seoul 03080, into macrophage-like cells through the MAPK signaling pathway. Gal-4 induced the phenotypic Korea. changes on monocytes by altering the expression of various surface molecules, and induced E-mail: [email protected] functional changes such as increased cytokine production and matrix metalloproteinase expression and reduced phagocytic capacity. -
Papers J Clin Pathol: First Published As 10.1136/Jcp.49.7.539 on 1 July 1996
Clin Pathol 1996;49:539-544 539 Papers J Clin Pathol: first published as 10.1136/jcp.49.7.539 on 1 July 1996. Downloaded from Differential expression of T cell antigens in normal peripheral blood lymphocytes: a quantitative analysis by flow cytometry L Ginaldi, N Farahat, E Matutes, M De Martinis, R Morilla, D Catovsky Abstract diagnosis by comparison with findings in Aims-To obtain reference values of the normal counterparts. level of expression of T cell antigens on ( Clin Pathol 1996;49:539-544) normal lymphocyte subsets in order to disclose differences which could reflect Keywords: flow cytometry, T cell antigens, peripheral their function or maturation stages, or blood lymphocytes. both. Methods-Peripheral blood from 15 healthy donors was processed by flow The most common use of flow cytometry is to cytometry with triple colour analysis. For determine the percent of "positive" or "nega- each sample phycoerythrin (PE) conju- tive" cells for each antigen in different cell gated CD2, CD4, CD5, CD8, and CD56 populations. However, valuable information is monoclonal antibodies were combined lost when the relative intensities of the positive with Cy5-R-phycoerythrin (TC) conju- cells, reflecting antigenic densities, are not considered. A cell population with a well gated CD3 and fluorescein isothiocyanate http://jcp.bmj.com/ (FITC) conjugated CD7; CD2- and defined phenotype, positive for one antigen, CD7-PE were also combined with might be heterogeneous with regard to its level CD3-TC and CD4-FITC. Standard mi- of expression. This may reflect different crobeads with different capacities to bind functional or maturational states, or both, or mouse immunoglobulins were used to identify subpopulations on the basis of the dif- convert the mean fluorescence intensity ferent numbers of molecules of antigen per cell. -
CD48 Is Critically Involved in Allergic Eosinophilic Airway Inflammation
CD48 Is Critically Involved in Allergic Eosinophilic Airway Inflammation Ariel Munitz,1 Ido Bachelet,1 Fred D. Finkelman,2 Marc E. Rothenberg,3 and Francesca Levi-Schaffer1,4 1Department of Pharmacology, School of Pharmacy, Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel; 2Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio; 3Division of Allergy and Immunology, Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio; and 4David R. Bloom Center for Pharmacology, Hebrew University of Jerusalem, Jerusalem, Israel Rationale: Despite ongoing research, the molecular mechanisms con- trolling asthma are still elusive. CD48 is a glycosylphosphatidylinositol- AT A GLANCE COMMENTARY anchored protein involved in lymphocyte adhesion, activation, and costimulation. Although CD48 is widely expressed on hematopoi- Scientific Knowledge on the Subject etic cells and commonly studied in the context of natural killer and CD48 is an activation molecule able to facilitate various cytotoxic T cell functions, its role in helper T cell type 2 settings cellular activities. Its role in asthma is unknown. has not been examined. Objectives: To evaluate the expression and function of CD48, CD2, and 2B4 in a murine model of allergic eosinophilic airway inflammation. What This Study Adds to the Field Methods: Allergic eosinophilic airway inflammation was induced by CD48 is upregulated in experimental asthma. Anti-CD48– ovalbumin (OVA)–alum sensitization and intranasal inoculation of based therapies may be useful for asthma and perhaps OVA or, alternatively, by repeated intranasal inoculation of Aspergil- various allergic diseases. lus fumigatus antigen in wild-type, STAT (signal transducer and acti- vator of transcription)-6–deficient, and IL-4/IL-13–deficient BALB/c mice. -
Signaling Expression by IL-7 and TCR Α Receptor Differential Regulation
Differential Regulation of Human IL-7 Receptor α Expression by IL-7 and TCR Signaling This information is current as Nuno L. Alves, Ester M. M. van Leeuwen, Ingrid A. M. of September 24, 2021. Derks and René A. W. van Lier J Immunol 2008; 180:5201-5210; ; doi: 10.4049/jimmunol.180.8.5201 http://www.jimmunol.org/content/180/8/5201 Downloaded from References This article cites 36 articles, 19 of which you can access for free at: http://www.jimmunol.org/content/180/8/5201.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 24, 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 Differential Regulation of Human IL-7 Receptor ␣ Expression by IL-7 and TCR Signaling1 Nuno L. Alves,2* Ester M. M. van Leeuwen,3*† Ingrid A. M. Derks,* and Rene´A. -
CD18) in a Patient with Leukocyte Adhesion Molecule (Leu-CAM) Deficiency
Point mutations impairing cell surface expression of the common beta subunit (CD18) in a patient with leukocyte adhesion molecule (Leu-CAM) deficiency. M A Arnaout, … , D G Tenen, D M Fathallah J Clin Invest. 1990;85(3):977-981. https://doi.org/10.1172/JCI114529. Research Article The leukocyte adhesion molecules CD11a/CD18, CD11b/CD18, and CD11c/CD18 (Leu-CAM) are members of the integrin receptor family and mediate crucial adhesion-dependent functions in leukocytes. The molecular basis for their deficient cell surface expression was sought in a patient suffering from severe and recurrent bacterial infections. Previous studies revealed that impaired cell surface expression of Leu-CAM is secondary to heterogeneous structural defects in the common beta subunit (CD18). Cloning and sequencing of complementary DNA encoding for CD18 in this patient revealed two mutant alleles, each representing a point mutation in the coding region of CD18 and resulting in an amino acid substitution. Each mutant allele results in impaired CD18 expression on the cell surface membrane of transfected COS M6 cells. One substitution involves an arginine residue (Arg593----cysteine) that is conserved in the highly homologous fourth cysteine-rich repeats of other mammalian integrin subfamilies. The other substitution involves a lysine residue (Lys196----threonine) located within another highly conserved region in integrins. These data identify crucial residues and regions necessary for normal cell surface expression of CD18 and possibly other integrin beta subunits and define a molecular basis for impaired cell surface expression of CD18 in this patient. Find the latest version: https://jci.me/114529/pdf Rapid Publication Point Mutations Impairing Cell Surface Expression of the Common ,B Subunit (CD18) in a Patient with Leukocyte Adhesion Molecule (Leu-CAM) Deficiency M. -
Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like, -
B Cell Checkpoints in Autoimmune Rheumatic Diseases
REVIEWS B cell checkpoints in autoimmune rheumatic diseases Samuel J. S. Rubin1,2,3, Michelle S. Bloom1,2,3 and William H. Robinson1,2,3* Abstract | B cells have important functions in the pathogenesis of autoimmune diseases, including autoimmune rheumatic diseases. In addition to producing autoantibodies, B cells contribute to autoimmunity by serving as professional antigen- presenting cells (APCs), producing cytokines, and through additional mechanisms. B cell activation and effector functions are regulated by immune checkpoints, including both activating and inhibitory checkpoint receptors that contribute to the regulation of B cell tolerance, activation, antigen presentation, T cell help, class switching, antibody production and cytokine production. The various activating checkpoint receptors include B cell activating receptors that engage with cognate receptors on T cells or other cells, as well as Toll-like receptors that can provide dual stimulation to B cells via co- engagement with the B cell receptor. Furthermore, various inhibitory checkpoint receptors, including B cell inhibitory receptors, have important functions in regulating B cell development, activation and effector functions. Therapeutically targeting B cell checkpoints represents a promising strategy for the treatment of a variety of autoimmune rheumatic diseases. Antibody- dependent B cells are multifunctional lymphocytes that contribute that serve as precursors to and thereby give rise to acti- cell- mediated cytotoxicity to the pathogenesis of autoimmune diseases