(CD244)/CD48 Interaction: Lys68 and Glu70 in the V Domain of 2B4 Are Critical for CD48 Binding and Functional Activation of NK Cells1
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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. -
Tools for Cell Therapy and Immunoregulation
RnDSy-lu-2945 Tools for Cell Therapy and Immunoregulation Target Cell TIM-4 SLAM/CD150 BTNL8 PD-L2/B7-DC B7-H1/PD-L1 (Human) Unknown PD-1 B7-1/CD80 TIM-1 SLAM/CD150 Receptor TIM Family SLAM Family Butyrophilins B7/CD28 Families T Cell Multiple Co-Signaling Molecules Co-stimulatory Co-inhibitory Ig Superfamily Regulate T Cell Activation Target Cell T Cell Target Cell T Cell B7-1/CD80 B7-H1/PD-L1 T cell activation requires two signals: 1) recognition of the antigenic peptide/ B7-1/CD80 B7-2/CD86 CTLA-4 major histocompatibility complex (MHC) by the T cell receptor (TCR) and 2) CD28 antigen-independent co-stimulation induced by interactions between B7-2/CD86 B7-H1/PD-L1 B7-1/CD80 co-signaling molecules expressed on target cells, such as antigen-presenting PD-L2/B7-DC PD-1 ICOS cells (APCs), and their T cell-expressed receptors. Engagement of the TCR in B7-H2/ICOS L 2Ig B7-H3 (Mouse) the absence of this second co-stimulatory signal typically results in T cell B7-H1/PD-L1 B7/CD28 Families 4Ig B7-H3 (Human) anergy or apoptosis. In addition, T cell activation can be negatively regulated Unknown Receptors by co-inhibitory molecules present on APCs. Therefore, integration of the 2Ig B7-H3 Unknown B7-H4 (Mouse) Receptors signals transduced by co-stimulatory and co-inhibitory molecules following TCR B7-H5 4Ig B7-H3 engagement directs the outcome and magnitude of a T cell response Unknown Ligand (Human) B7-H5 including the enhancement or suppression of T cell proliferation, B7-H7 Unknown Receptor differentiation, and/or cytokine secretion. -
CD2 Molecules Redistribute to the Uropod During T Cell Scanning: Implications for Cellular Activation and Immune Surveillance
CD2 molecules redistribute to the uropod during T cell scanning: Implications for cellular activation and immune surveillance Elena V. Tibaldi*†, Ravi Salgia†‡, and Ellis L. Reinherz*†§ *Laboratory of Immunobiology and ‡Division of Adult Oncology, Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, and †Department of Medicine, Harvard Medical School, Boston, MA 02115 Communicated by Stuart F. Schlossman, Dana-Farber Cancer Institute, Boston, MA, April 9, 2002 (received for review February 14, 2002) Dynamic binding between CD2 and CD58 counter-receptors on op- cells, whereas its counter-receptor CD58 is expressed on a posing cells optimizes immune recognition through stabilization of diverse array of nucleated and non-nucleated cells including cell–cell contact and juxtaposition of surface membranes at a distance APCs and stromal cells (reviewed in refs. 11 and 12). CD2 suitable for T cell receptor–ligand interaction. Digitized time-lapse functions in both T cell adhesion and activation processes (13). Ϸ differential interference contrast and immunofluorescence micros- Of note, the weak affinity of the CD2-CD58 interaction (Kd copy on living cells now show that this binding also induces T cell 1 M) is associated with remarkably fast on and off rates that polarization. Moreover, CD2 can facilitate motility of T cells along foster rapid and extensive exchange between CD2 and CD58 antigen-presenting cells via a movement referred to as scanning. Both partners on opposing cell surfaces (14–16). These biophysical activated CD4 and CD8 T cells are able to scan antigen-presenting cells characteristics are reminiscent of the selectin–ligand interactions surfaces in the absence of cognate antigen. -
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. -
Folate Receptor Β Regulates Integrin Cd11b/CD18 Adhesion of a Macrophage Subset to Collagen
Folate Receptor β Regulates Integrin CD11b/CD18 Adhesion of a Macrophage Subset to Collagen This information is current as Christian Machacek, Verena Supper, Vladimir Leksa, Goran of September 25, 2021. Mitulovic, Andreas Spittler, Karel Drbal, Miloslav Suchanek, Anna Ohradanova-Repic and Hannes Stockinger J Immunol 2016; 197:2229-2238; Prepublished online 17 August 2016; doi: 10.4049/jimmunol.1501878 Downloaded from http://www.jimmunol.org/content/197/6/2229 Supplementary http://www.jimmunol.org/content/suppl/2016/08/17/jimmunol.150187 Material 8.DCSupplemental http://www.jimmunol.org/ References This article cites 49 articles, 23 of which you can access for free at: http://www.jimmunol.org/content/197/6/2229.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 25, 2021 • 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 © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Folate Receptor b Regulates Integrin CD11b/CD18 Adhesion of a Macrophage Subset to Collagen Christian Machacek,* Verena Supper,* Vladimir Leksa,*,† Goran Mitulovic,‡ Andreas Spittler,x Karel Drbal,{,1 Miloslav Suchanek,{ Anna Ohradanova-Repic,* and Hannes Stockinger* Folate, also known as vitamin B9, is necessary for essential cellular functions such as DNA synthesis, repair, and methylation. -
Response Gene Expression That Modulates T Cell Induces a Differential Cytokine Tuberculosis Mycobacterium Dendritic Cells with I
Infection of Human Macrophages and Dendritic Cells with Mycobacterium tuberculosis Induces a Differential Cytokine Gene Expression That Modulates T Cell This information is current as Response of September 24, 2021. Elena Giacomini, Elisabetta Iona, Lucietta Ferroni, Minja Miettinen, Lanfranco Fattorini, Graziella Orefici, Ilkka Julkunen and Eliana M. Coccia J Immunol 2001; 166:7033-7041; ; Downloaded from doi: 10.4049/jimmunol.166.12.7033 http://www.jimmunol.org/content/166/12/7033 http://www.jimmunol.org/ References This article cites 51 articles, 22 of which you can access for free at: http://www.jimmunol.org/content/166/12/7033.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 24, 2021 • 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 © 2001 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Infection of Human Macrophages and Dendritic Cells with Mycobacterium tuberculosis Induces a Differential Cytokine Gene Expression That Modulates T Cell Response1 Elena Giacomini,* Elisabetta Iona,† Lucietta Ferroni,* Minja Miettinen,‡ Lanfranco Fattorini,† Graziella Orefici,† Ilkka Julkunen,‡ and Eliana 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, -
Cytokine Regulation in Human CD4 T Cells by the Aryl Hydrocarbon
www.nature.com/scientificreports OPEN Cytokine Regulation in Human CD4 T Cells by the Aryl Hydrocarbon Receptor and Gq-Coupled Received: 17 November 2017 Accepted: 9 July 2018 Receptors Published: xx xx xxxx Jeremy P. McAleer1, Jun Fan2, Bryanna Roar1, Donald A. Primerano2 & James Denvir2 Th17 cells contribute to host defense on mucosal surfaces but also provoke autoimmune diseases when directed against self-antigens. Identifying therapeutic targets that regulate Th17 cell diferentiation and/or cytokine production has considerable value. Here, we study the aryl hydrocarbon receptor (AhR)- dependent transcriptome in human CD4 T cells treated with Th17-inducing cytokines. We show that the AhR reciprocally regulates IL-17 and IL-22 production in human CD4 T cells. Global gene expression analysis revealed that AhR ligation decreased IL21 expression, correlating with delayed upregulation of RORC during culture with Th17-inducing cytokines. Several of the AhR-dependent genes have known roles in cellular assembly, organization, development, growth and proliferation. We further show that expression of GPR15, GPR55 and GPR68 positively correlates with IL-22 production in the presence of the AhR agonist FICZ. Activation of GPR68 with the lorazepam derivative ogerin resulted in suppression of IL-22 and IL-10 secretion by T cells, with no efect on IL-17. Under neutral Th0 conditions, ogerin and the Gq/11 receptor inhibitor YM254890 blunted IL-22 induction by FICZ. These data reveal the AhR- dependent transcriptome in human CD4 T cells and suggest the mechanism through which the AhR regulates T cell function may be partially dependent on Gq-coupled receptors including GPR68. -
The Immunological Synapse and CD28-CD80 Interactions Shannon K
© 2001 Nature Publishing Group http://immunol.nature.com ARTICLES The immunological synapse and CD28-CD80 interactions Shannon K. Bromley1,Andrea Iaboni2, Simon J. Davis2,Adrian Whitty3, Jonathan M. Green4, Andrey S. Shaw1,ArthurWeiss5 and Michael L. Dustin5,6 Published online: 19 November 2001, DOI: 10.1038/ni737 According to the two-signal model of T cell activation, costimulatory molecules augment T cell receptor (TCR) signaling, whereas adhesion molecules enhance TCR–MHC-peptide recognition.The structure and binding properties of CD28 imply that it may perform both functions, blurring the distinction between adhesion and costimulatory molecules. Our results show that CD28 on naïve T cells does not support adhesion and has little or no capacity for directly enhancing TCR–MHC- peptide interactions. Instead of being dependent on costimulatory signaling, we propose that a key function of the immunological synapse is to generate a cellular microenvironment that favors the interactions of potent secondary signaling molecules, such as CD28. The T cell receptor (TCR) interaction with complexes of peptide and as CD2 and CD48, which suggests that CD28 might have a dual role as major histocompatibility complex (pMHC) is central to the T cell an adhesion and a signaling molecule4. Coengagement of CD28 with response. However, efficient T cell activation also requires the partici- the TCR has a number of effects on T cell activation; these include pation of additional cell-surface receptors that engage nonpolymorphic increasing sensitivity to TCR stimulation and increasing the survival of ligands on antigen-presenting cells (APCs). Some of these molecules T cells after stimulation5. CD80-transfected APCs have been used to are involved in the “physical embrace” between T cells and APCs and assess the temporal relationship of TCR and CD28 signaling, as initiat- are characterized as adhesion molecules. -
Proliferation by 2B4/CD48 Interactions T Cell
Cutting Edge: Regulation of CD8+ T Cell Proliferation by 2B4/CD48 Interactions Taku Kambayashi, Erika Assarsson, Benedict J. Chambers and Hans-Gustaf Ljunggren This information is current as of September 29, 2021. J Immunol 2001; 167:6706-6710; ; doi: 10.4049/jimmunol.167.12.6706 http://www.jimmunol.org/content/167/12/6706 Downloaded from References This article cites 23 articles, 12 of which you can access for free at: http://www.jimmunol.org/content/167/12/6706.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • 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 by guest on September 29, 2021 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 © 2001 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. ● Cutting Edge: Regulation of CD8؉ T Cell Proliferation by 2B4/CD48 Interactions1 Taku Kambayashi,2* Erika Assarsson,2* Benedict J. Chambers,* and Hans-Gustaf Ljunggren3*† To date, the only known 2B4-binding molecule is CD48. Bind- The biological function of 2B4, a CD48-binding molecule ex- ing studies have shown that CD48 has a 5–10 times stronger af- pressed on T cells with an activation/memory phenotype, is not finity for 2B4 than for CD2 (7, 8). -
REVIEW Dendritic Cell-Based Vaccine
Leukemia (1999) 13, 653–663 1999 Stockton Press All rights reserved 0887-6924/99 $12.00 http://www.stockton-press.co.uk/leu REVIEW Dendritic cell-based vaccine: a promising approach for cancer immunotherapy K Tarte1 and B Klein1,2 1INSERM U 475, Montpellier; and 2Unit For Cellular Therapy, CHU Saint Eloi, Montpellier, France The unique ability of dendritic cells to pick up antigens and to + + and interstitial DC pick up antigens (Ag) in peripheral tissues activate naive and memory CD4 and CD8 T cells raised the and migrate to lymphoid organs through lymphatic vessels in possibility of using them to trigger a specific anti-tumor 8 immunity. If numerous studies have shown a major interest in response to inflammatory stimuli. Activated mature DC, dendritic cell-based vaccines for cancer immunotherapy in ani- which express CD1a and CD83 antigens, represent the latter mal models, only a few have been carried out in human can- stage of LC and interstitial DC maturation. According to their cers. In this review, we describe recent findings in the biology high expression of MHC class I, MHC class II and costimu- of dendritic cells that are important to generate anti-tumor cyto- latory molecules, they present, efficiently, Ag-derived peptides toxic T cells in vitro and we also detail clinical studies reporting to CD4+ and CD8+ T lymphocytes in lymph node T cell areas the obtention of specific immunity to human cancers in vivo using reinfusion of dendritic cells pulsed with tumor antigens. (Figure 1). Recently, another subset of DC was identified on Keywords: dendritic cells; cancer; immunotherapy the basis of their high expression of the interleukin-3 receptor alpha chain (IL-3R␣hi). -
The Role of the CD58 Locus in Multiple Sclerosis
The role of the CD58 locus in multiple sclerosis Philip L. De Jagera,b,c,1, Clare Baecher-Allana, Lisa M. Maiera,c, Ariel T. Arthurd, Linda Ottobonia,c, Lisa Barcellose, Jacob L. McCauleyf, Stephen Sawcerg, An Gorish, Janna Saarelai, Roman Yelenskyc,j, Alkes Pricec,k, Virpi Leppai, Nick Pattersonc, Paul I. W. de Bakkerb,c, Dong Trana,c, Cristin Aubina,c, Susan Pobywajloa, Elizabeth Rossina,c, Xinli Huc, Charles W. Ashleya, Edwin Choyc,j, John D. Riouxc,l, Margaret A. Pericak-Vancef, Adrian Ivinsonm, David R. Boothn, Graeme J. Stewartn, Aarno Palotiec,h, Leena Peltonenc,h,Be´ ne´ dicte Duboisg, Jonathan L. Haineso, Howard L. Weinera, Alastair Compstong, Stephen L. Hauserp,q, Mark J. Dalyc,j, David Reichc,j, Jorge R. Oksenbergp,q, and David A. Haflera,c. aDivision of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115; bPartners Center for Personalized Genetic Medicine, Boston, MA 02115; cProgram in Medical and Population Genetics, Broad Institute of Harvard University and Massachusetts Institute of Technology, Cambridge, MA 02139; dDepartment of Medicine and the Nerve Research Foundation, University of Sydney, Sydney NSW 2145, Australia; eDivision of Epidemiology, School of Public Health, University of California, Berkeley, CA 94720-7360; fMiami Institute for Human Genomics, Miller School of Medicine, University of Miami, Miami, FL 33136; gDepartment of Clinical Neurosciences, Addenbrooke’s Hospital, University of Cambridge, Box 165, Hills Road, Cambridge CB2 2QQ,