Resting Peripheral Blood B Cells Presentation of Immune Complexes
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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. -
The Ligands for Human Igg and Their Effector Functions
antibodies Review The Ligands for Human IgG and Their Effector Functions Steven W. de Taeye 1,2,*, Theo Rispens 1 and Gestur Vidarsson 2 1 Sanquin Research, Dept Immunopathology and Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, 1066 CX Amsterdam, The Netherlands; [email protected] 2 Sanquin Research, Dept Experimental Immunohematology and Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, 1066 CX Amsterdam, The Netherlands; [email protected] * Correspondence: [email protected] Received: 26 March 2019; Accepted: 18 April 2019; Published: 25 April 2019 Abstract: Activation of the humoral immune system is initiated when antibodies recognize an antigen and trigger effector functions through the interaction with Fc engaging molecules. The most abundant immunoglobulin isotype in serum is Immunoglobulin G (IgG), which is involved in many humoral immune responses, strongly interacting with effector molecules. The IgG subclass, allotype, and glycosylation pattern, among other factors, determine the interaction strength of the IgG-Fc domain with these Fc engaging molecules, and thereby the potential strength of their effector potential. The molecules responsible for the effector phase include the classical IgG-Fc receptors (FcγR), the neonatal Fc-receptor (FcRn), the Tripartite motif-containing protein 21 (TRIM21), the first component of the classical complement cascade (C1), and possibly, the Fc-receptor-like receptors (FcRL4/5). Here we provide an overview of the interactions of IgG with effector molecules and discuss how natural variation on the antibody and effector molecule side shapes the biological activities of antibodies. The increasing knowledge on the Fc-mediated effector functions of antibodies drives the development of better therapeutic antibodies for cancer immunotherapy or treatment of autoimmune diseases. -
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. -
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. -
Anti-CD40 Antibody KPL-404 Inhibits T Cell
Marken et al. Arthritis Research & Therapy (2021) 23:5 https://doi.org/10.1186/s13075-020-02372-z RESEARCH ARTICLE Open Access Anti-CD40 antibody KPL-404 inhibits T cell- mediated activation of B cells from healthy donors and autoimmune patients John Marken1, Sujatha Muralidharan2* and Natalia V. Giltiay1* Abstract Background: CD40-CD40L is a key co-stimulatory pathway for B cell activation. As such, its blockade can inhibit pathogenic B cell responses in autoimmune diseases, such as Sjogren’s syndrome (SjS) and systemic lupus erythematosus (SLE). In this study, we examined the in vitro effects of KPL-404, a humanized anti-CD40 monoclonal antibody (Ab), on primary human B cells derived from either healthy donors (HD) or autoimmune patients and compared them to the effects of G28-5, a partially antagonistic anti-CD40 antibody. Methods: PBMCs from HD or SjS and SLE patients were cultured in high-density cell cultures in the presence of IgG4 isotype control or anti-CD40 Abs KPL-404 or G28-5. Cells were stimulated with anti-CD3/CD28 cross-linking reagent ImmunoCult (IC) to induce CD40L-CD40-mediated B cell responses. B cell proliferation and activation, measured by dilution of proliferation tracker dye and the upregulation of CD69 and CD86, respectively, were assessed by flow cytometry. Anti-CD40 Ab cell-internalization was examined by imaging flow cytometry. Cytokine release in the PBMC cultures was quantified by bead-based multiplex assay. Results: KPL-404 binds to CD40 expressed on different subsets of B cells without inducing cell depletion, or B cell proliferation and activation in in vitro culture. -
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. -
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. -
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. -
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. -
Slan Monocytes and Macrophages Mediate CD20-Dependent B-Cell
Published OnlineFirst May 10, 2018; DOI: 10.1158/0008-5472.CAN-17-2344 Cancer Tumor Biology and Immunology Research slanþ Monocytes and Macrophages Mediate CD20-Dependent B-cell Lymphoma Elimination via ADCC and ADCP William Vermi1,2, Alessandra Micheletti3, Giulia Finotti3, Cristina Tecchio4, Federica Calzetti3, Sara Costa3, Mattia Bugatti1, Stefano Calza5, Claudio Agostinelli6, Stefano Pileri7, Piera Balzarini1, Alessandra Tucci8, Giuseppe Rossi8, Lara Furlani4, Giuseppe Todeschini4, Alberto Zamo9, Fabio Facchetti1, Luisa Lorenzi1, Silvia Lonardi1, and Marco A. Cassatella3 Abstract þ Terminal tissue differentiation and function of slan monocytes in cancer þ + + is largely unexplored. Our recent studies demonstrated that slan mono- slan monocyte slan macrophage cytes differentiate into a distinct subset of dendritic cells (DC) in human CD16A þ tonsils and that slan cells colonize metastatic carcinoma-draining lymph CD32 nodes. Herein, we report by retrospective analysis of multi-institutional þ CD16A CD64 cohorts that slan cells infiltrate various types of non-Hodgkin lymphomas = RTX (NHL), particularly the diffuse large B-cell lymphoma (DLBCL) group, CD20 þ CD20 including the most aggressive, nodal and extranodal, forms. Nodal slan cells displayed features of either immature DC or macrophages, in the latter case ingesting tumor cells and apoptotic bodies. We also found in patients þ þ with DLBCL that peripheral blood slan monocytes, but not CD14 monocytes, increased in number and displayed highly efficient rituxi- Lymphoma cell Lymphoma cell mab-mediated antibody-dependent cellular cytotoxicity, almost equivalent + RTX þ to that exerted by NK cells. Notably, slan monocytes cultured in condi- tioned medium from nodal DLBCL (DCM) acquired a macrophage-like + RTX phenotype, retained CD16 expression, and became very efficient in ritux- imab-mediated antibody-dependent cellular phagocytosis (ADCP). -
CD32+ and PD-1+ Lymph Node CD4 T Cells Support Persistent HIV-1
bioRxiv preprint doi: https://doi.org/10.1101/329938; this version posted May 24, 2018. 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. 1 CD32+ and PD-1+ Lymph Node CD4 T Cells Support Persistent HIV-1 2 Transcription in Treated Aviremic Individuals 3 Alessandra Notoa, Francesco A. Procopioa, Riddhima Bangaa, Madeleine Suffiottia, Jean-Marc 4 Corpatauxb, Matthias Cavassinic, Craig Fenwicka, Raphael Gottardod, Matthieu Perreaua, 5 Giuseppe Pantaleoa,e# 6 7 aService of Immunology and Allergy, Lausanne University Hospital, University of Lausanne, 8 Lausanne, Switzerland 9 bService of Vascular Surgery, Lausanne University Hospital, University of Lausanne, Lausanne, 10 Switzerland 11 cService of Infectious Diseases, Lausanne University Hospital, University of Lausanne, 12 Lausanne, Switzerland 13 dVaccine and Infectious Disease Divisions, Fred Hutchinson Cancer Research Center, Seattle, 14 Washington, USA 15 eSwiss Vaccine Research Institute, Lausanne University Hospital, University of Lausanne, 16 Lausanne, Switzerland 17 Running Head: Role of CD32 and PD-1 in Defining the HIV Reservoir 18 #Address correspondence to Giuseppe Pantaleo, [email protected] 19 Word count for the abstract: 318 Word count for the text: 4130 20 1 bioRxiv preprint doi: https://doi.org/10.1101/329938; this version posted May 24, 2018. 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. 21 ABSTRACT 22 A recent study conducted in blood has proposed CD32 as the marker identifying the ‘elusive’ HIV 23 reservoir. We have investigated the distribution of CD32+ CD4 T cells in blood and lymph nodes 24 (LNs) of healthy HIV-1 uninfected, viremic untreated and long-term treated HIV-1 infected 25 individuals and their relationship with PD-1+ CD4 T cells.