Immunohistochemical Expression of CD23 and CD40 May Identify Prognostically Favorable Subgroups of Diffuse Large B-Cell Lymphoma: a Nordic Lymphoma Group Study1
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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. -
ORIGINAL ARTICLE Flow Cytometric Protein Expression Profiling As a Systematic Approach for Developing Disease-Specific Assays
Leukemia (2006) 20, 2102–2110 & 2006 Nature Publishing Group All rights reserved 0887-6924/06 $30.00 www.nature.com/leu ORIGINAL ARTICLE Flow cytometric protein expression profiling as a systematic approach for developing disease-specific assays: identification of a chronic lymphocytic leukaemia-specific assay for use in rituximab-containing regimens AC Rawstron, R de Tute, AS Jack and P Hillmen Haematological Malignancy Diagnostic Service (HMDS), Leeds Teaching Hospitals, Leeds, UK Depletion of disease below the levels detected by sensitive sustained remissions only occur in patients achieving an MRD- minimal residual disease (MRD) assays is associated with negative complete response.12 Therefore MRD is increasingly prolonged survival in chronic lymphocytic leukaemia (CLL). being used as an end point for therapeutic trials, and several Flow cytometric MRD assays are now sufficiently sensitive and rapid to guide the duration of therapy in CLL, but generally rely studies are now using the assessment of MRD to define the on assessment of CD20 expression, which cannot be accurately duration of therapy. measured during and after therapeutic approaches containing Approaches using allele-specific oligonucleotide polymerase rituximab. The aim of this study was to use analytical software chain reaction (ASO-PCR) to the immunoglobulin gene of the developed for microarray analysis to provide a systematic B-CLL cell are generally accepted to show the highest sensitivity approach for MRD flow assay development. Samples from CLL for MRD detection. However, more recent four-colour ap- patients (n ¼ 49), normal controls (n ¼ 21) and other B-lympho- proaches show sensitivities nearing that of ASO-PCR6,11,13 with proliferative disorders (n ¼ 12) were assessed with a panel of 66 antibodies. -
New Advances in Leukaemia Immunotherapy by the Use of Chimeric Artificial Antigen Receptors
Biagi et al. Italian Journal of Pediatrics 2011, 37:46 http://www.ijponline.net/content/37/1/46 ITALIAN JOURNAL OF PEDIATRICS REVIEW Open Access New advances in leukaemia immunotherapy by the use of Chimeric Artificial Antigen Receptors (CARs): state of the art and perspectives for the near future Ettore Biagi*, Virna Marin, Greta Maria Paola Giordano Attianese, Irene Pizzitola, Sarah Tettamanti, Elisabetta Cribioli and Andrea Biondi Abstract Leukaemia immunotherapy represents a fascinating and promising field of translational research, particularly as an integrative approach of bone marrow transplantation. Adoptive immunotherapy by the use of donor-derived expanded leukaemia-specific T cells has showed some kind of clinical response, but the major advance is nowadays represented by gene manipulation of donor immune cells, so that they acquire strict specificity towards the tumour target and potent lytic activity, followed by significant proliferation, increased survival and possibly anti- tumour memory state. This is achieved by gene insertion of Chimeric T-cell Antigen Receptors (CARs), which are artificial molecules containing antibody-derived fragments (to bind the specific target), joined with potent signalling T-Cell Receptor (TCR)-derived domains that activate the manipulated cells. This review will discuss the main application of this approach particularly focusing on the paediatric setting, raising advantages and disadvantages and discussing relevant perspectives of use in the nearest future. Keywords: Leukaemia immunotherapy, -
Genetic Modification of Human T Lymphocytes for the Treatment of Hematologic Malignancies
REVIEW ARTICLE Genetic modification of human T lymphocytes for the treatment of hematologic malignancies Valentina Hoyos, 1,2 Barbara Savoldo, 1,2 and Gianpietro Dotti 1,2,4 1Center for Cell and Gene Therapy, Baylor College of Medicine, Houston; 2Department of Medicine, Baylor College of Medicine, Houston; 3Department of Pediatrics, Texas Children’s Hospital, Houston; and 4Department of Immunology, Baylor College of Medicine, Houston, USA ABSTRACT Modern chemotherapy regimens and supportive care have post-transplant lymphomas and Hodgkin’s lymphomas. produced remarkable improvements in the overall survival of Because of this compelling clinical evidence and the con - patients with hematologic malignancies. However, the comitant development of methodologies for robust gene development of targeted small molecules, monoclonal anti - transfer to human T lymphocytes, the field has rapidly bodies, and biological therapies that demonstrate greater evolved, offering new opportunities to extend T-cell based efficacy and lower toxicity remains highly desirable in hema - therapies. This review summarizes the most recent biologi - tology, and oncology in general. In the context of biological cal and clinical developments using genetically manipulated therapies, T-lymphocyte based treatments have enormous T cells for the treatment of hematologic malignancies. potential. Donor lymphocyte infusion in patients relapsed after allogeneic hematopoietic stem cell transplant pioneered Key words: immunotherapy, cytotoxic T lymphocytes, gene the concept that T lymphocytes can effectively control transfer, chimeric antigen receptor, suicide gene. tumor growth, and this was then followed by the develop - ment of cell culture strategies to generate T lymphocytes Citation: Hoyos V, Savoldo B, and Dotti G. Genetic modification of with selective activity against tumor cells. -
5-Mediated ERK Activation and Adhesion-Independent Growth of Human Pre-B Cell Lines
Leukemia (2009) 23, 1807–1817 & 2009 Macmillan Publishers Limited All rights reserved 0887-6924/09 $32.00 www.nature.com/leu ORIGINAL ARTICLE SDF-1 and PDGF enhance avb5-mediated ERK activation and adhesion-independent growth of human pre-B cell lines M Acharya1,3, AL Edkins1,4, BW Ozanne2 and W Cushley1 1Division of Molecular and Cellular Biology, Faculty of Biomedical and Life Sciences, University of Glasgow, Glasgow, Scotland, UK and 2Cancer Research-UK Beatson Laboratories, Garscube Estate, Glasgow, Scotland, UK CD23 acts through the avb5 integrin to promote growth of and differentiation of centrocytes by binding to CD21.7–9 human pre-B cell lines in an adhesion-independent manner. Plasma sCD23 levels are low in normal subjects, but high avb5 is expressed on normal B-cell precursors in the bone levels are reported in inflammatory disorders such as rheuma- marrow. Soluble CD23 (sCD23), short CD23-derived peptides 10 containing the arg-lys-cys (RKC) motif recognized by avb5 and toid arthritis and systemic lupus erythmatosus. Particularly anti-avb5 monoclonal antibodies (MAbs) all sustain growth of high levels of sCD23 with prognostic value are a hallmark of pre-B cell lines. The chemokine stromal cell-derived factor-1 B-cell chronic lymphoblastic leukaemia.11 The avb5 integrin, (SDF-1) regulates key processes during B-cell development. a member of the vitronectin receptor family, is expressed by SDF-1 enhanced the growth-sustaining effect driven by ligation bone marrow B-cell precursors.2 The vitronectin receptor family of avb5 with anti-avb5 MAb 15F-11, sCD23 or CD23-derived a RKC-containing peptides. -
Flow Cytometric Analysis of B-Cell Lymphoproliferative Disorders
Flow cytometric analysis of B-cell lymphoproliferative disorders David M. Dorfman, M.D., Ph.D. Department of Pathology Brigham and Women’s Hospital and Harvard Medical School Boston, MA Objectives • Review basic principles of flow cytometric immunophenotypic analysis of B cell lymphoproliferative disorders • Discuss recent studies to overcome limitations and shortcomings – New markers – New methods Incidence of B-cell neoplasms, United States Subtype Incidence rate 2011-2012 New cases, 2016 per 100,000 Lymphoid neoplasms 34.4 136,960 Lymphoid neoplasms, B 29.0 93.3% 117,470 B-LL/L 1.4 82.2% 4,930 CLL/SLL 5.1 20,980 FL 3.4 13,960 DLBCL 6.3 27,650 MM 5.9 24,280 Lymphoid neoplasms, T/NK 2.1 8,380 T-LL/L 0.3 1,070 T-PLL <0.1 160 T-LGL 0.2 670 ATL/L <0.1 180 Teras et al. CA Cancer J Clin 2016; 66:443-459 (North American AssociationTeras of et Central al. CA Cancer Cancer Registries) J Clin 2016; 66:443-459 (North American Association of Central Cancer Registries) SS <0.1 Teras et al. CA Cancer J Clin70 2016; 66:443-459 (North American Association of Central Cancer Registries) 94% WHO revised 4th ed., 2017 Flow cytometric analysis of B-cell lymphoproliferative disorders • B-cell antigen expression (CD19, CD20, CD22) • Monoclonal surface immunoglobulin κ or λ light chain expression (or absence of surface immunoglobulin) • Expression of additional B-cell antigens or other antigens, including abnormal expression levels • Presence of cells with abnormal light scatter characteristics ( high forward scatter or side scatter) B-ALL MCL FL, HL MZL, CLL, MM LPL DLBCL DLBCL WHO revised 4th ed. -
Immunology Focus Summer | 2006 Immunology FOCUS
R&D Systems Immunology Focus summer | 2006 Immunology FOCUS Inside page 2 Signal Transduction: Kinase & Phosphatase Reagents page 3 Lectin Family page 4 Regulatory T Cells page 5 Natural Killer Cells page 6 Innate Immunity & Dendritic Cells page 7 Co-Stimulation/-Inhibition The B7 Family & Associated Molecules page 8 Proteome Profiler™ Phospho-Immunoreceptor Array ITAM/ITIM-Associated Receptors www.RnDSystems.com Please visit our website @ www.RnDSystems.com for product information and past issues of the Focus Newsletter: Cancer, Neuroscience, Cell Biology, and more. Quality | Selec tion | Pe rformance | Result s Cancer Development Endocrinology Immunology Neuroscience Proteases Stem Cells Signal Transduction: Kinase & Phosphatase Reagents Co-inhibitory PD-L2/PD-1 signaling & SHP-2 phosphatase KINASE & PHOSPHATASE RESEARCH REAGENTS Regulation of MAP kinase (MAPK) signaling Kinases Phosphatases pathways is critical for T cell development, MOLECULE ANTIBODIES ELISAs/ASSAYS MOLECULE ANTIBODIES ELISAs/ASSAYS activation, differentiation, and death. MAPKs Akt Family H M R H M R Alkaline Phosphatase* H M R are activated by the dual phosphorylation of threonine and tyrosine residues resulting in AMPK H M R Calcineurin A, B H M R subsequent transcription factor activation. ATM H M R H CD45 H M H M The MAPK signaling pathway in T cells can be CaM Kinase II Ms CDC25A, B* H M R triggered by cytokines, growth factors, and CDC2 H M R DARPP-32 M R ligands for transmembrane receptors. Chk1, 2 H M R H M R DEP-1/CD148* H M R H Ligation of the T cell receptor (TCR)/CD3 ERK1, 2 H M R H M R LAR H M R complex results in rapid activation of PI 3- kinase, which leads to Akt and MAPK ERK3 H Lyp H activation. -
Mouse and Human Fcr Effector Functions
Pierre Bruhns Mouse and human FcR effector € Friederike Jonsson functions Authors’ addresses Summary: Mouse and human FcRs have been a major focus of Pierre Bruhns1,2, Friederike J€onsson1,2 attention not only of the scientific community, through the cloning 1Unite des Anticorps en Therapie et Pathologie, and characterization of novel receptors, and of the medical commu- Departement d’Immunologie, Institut Pasteur, Paris, nity, through the identification of polymorphisms and linkage to France. disease but also of the pharmaceutical community, through the iden- 2INSERM, U760, Paris, France. tification of FcRs as targets for therapy or engineering of Fc domains for the generation of enhanced therapeutic antibodies. The Correspondence to: availability of knockout mouse lines for every single mouse FcR, of Pierre Bruhns multiple or cell-specific—‘a la carte’—FcR knockouts and the Unite des Anticorps en Therapie et Pathologie increasing generation of hFcR transgenics enable powerful in vivo Departement d’Immunologie approaches for the study of mouse and human FcR biology. Institut Pasteur This review will present the landscape of the current FcR family, 25 rue du Docteur Roux their effector functions and the in vivo models at hand to study 75015 Paris, France them. These in vivo models were recently instrumental in re-defining Tel.: +33145688629 the properties and effector functions of FcRs that had been over- e-mail: [email protected] looked or discarded from previous analyses. A particular focus will be made on the (mis)concepts on the role of high-affinity Acknowledgements IgG receptors in vivo and on results from antibody engineering We thank our colleagues for advice: Ulrich Blank & Renato to enhance or abrogate antibody effector functions mediated by Monteiro (FacultedeMedecine Site X. -
LECTURE 07 Immune Cells Surface Receptors and Their Functions
LECTURE: 07 Title: IMMUNE CELL SURFACE RECEPTORS AND THEIR FUNCTIONS LEARNING OBJECTIVES: The student should be able to: • The chemical nature of the cellular surface receptors. • Define the location of the cellular receptors. • Enumerate the different given terms for the word "receptor". • Define the term "CD" marker. • Describe the location of the immune receptors. • Classify the cellular receptors according to the information they offer. • Classify the cellular receptors according to their families. • Enumerate some common immunoglobulin receptors. • Enumerate some common complement receptors. • Enumerate some adhesion molecules receptors. • Enumerate the main functions of the immune cell receptors. • Realize the importance of the immune receptors. LECTURE REFRENCE: 1. TEXTBOOK: ROITT, BROSTOFF, MALE IMMUNOLOGY. 6th edition. pp. 29, 143, 76, 77, 78, 221, 325. 2. TEXTBOOK: ABUL K. ABBAS. ANDREW H. LICHTMAN. CELLULAR AND MOLECULAR IMMUNOLOGY. 5TH EDITION. Chapter. 6 .pg 105. Chapter 4. pg 65- 80. 1 Lymphocytes can be identified by characteristic markers Lymphocytes and other leukocytes express different surface molecules which can be used for distinguishing cell population. A systemic nomenclature called the CD system has been developed, in which the term CD refers to (cluster of designation). These different cell surface molecules are detected with specific monoclonal antibodies, each of these molecules are given CD number. Molecular markers can be further defined according to the information they offer about the cell. For example; A. Lineage markers are exclusive to a particular cell line, e.g., CD3, which is found only on T cells. B. Maturation markers are transiently expressed during cell differentiation, e.g., CD1, which is only found on cells developing in thymus and is not present on peripheral T cells. -
Reproducible Diagnosis of CLL by Flow Cytometry: an ERIC & ESCCA
Reproducible diagnosis of CLL by flow cytometry: an ERIC & ESCCA harmonisation project Andy C. Rawstron, Karl-Anton Kreuzer, Asha Soosapilla, Martin Spacek, Peter Gambell, Neil McIver-Brown, Katherina Psarra, Maria Arroz, Raffaella Milani, Javier de la Serna, M. Teresa Cedena, Ozren Jaksic, Josep Nomdedeu, Carol Moreno, Gian Matteo Rigolin, Antonio Cuneo, Preben Johansen, Hans Johnsen, Richard Rosenquist Brandell, Carston Utoft Niemann, David Westerman, Marek Trneny, Stephen Mulligan, Peter Hillmen, David Oscier, Michael Hallek, Paolo Ghia, Emili Montserrat. On behalf of the European Research Initiated on CLL (ERIC) and the European Society for Clinical Cell Analysis (ESCCA) Current criteria: flexibility in marker expression • WHO criteria: • IWCLL guidelines: • CLL cells usually co-express CD5 and • CLL cells co-express the T-cell CD23 antigen CD5 and B-cell surface • Using flow cytometry, the tumour cells antigens CD19, CD20, and CD23. express dim surface IgM/IgD, CD20, CD22, CD5, CD19, CD79a, CD23, CD43 • The levels of surface Ig, CD20, & and CD11c (weak). CD10 is negative CD79b are characteristically low. and FMC& and CD79b are usually negative or weakly expressed in typical • Each clone is restricted to expression CLL. of either kappa or lambda. • Some cases may have an atypical • Variations of the intensity of immunophenotype (e.g. CD5- or expression of these markers may CD23-, FMC7+ or CD11c+, strong sIg, or CD79b+). exist and do not prevent inclusion of a patient in clinical trials for CLL. Trial cases referred to a central lab: ~2-5% not CLL & ~2-5% sub-optimal for MRD monitoring but this may vary according to trial treatment options • ADMIRE/ARCTIC trial: FCR-based treatment (n=421) • 97% typical phenotype (2% with no CD200 or CD43 expression) • 3% CD23neg, usually with additional aberrant markers but no t(11;14). -
Characterization of a 23-Kda Protein Associated with CD40 TOMOHIRO MORIO, SILVA HANISSIAN, and RAIF S
Proc. Natl. Acad. Sci. USA Vol. 92, pp. 11633-11636, December 1995 Immunology Characterization of a 23-kDa protein associated with CD40 TOMOHIRO MORIO, SILVA HANISSIAN, AND RAIF S. GEHA* Division of Immunology, Children's Hospital, and Department of Pediatrics, Harvard Medical School, Boston, MA 02115 Communicated by Mary Ellen Avery, Harvard Medical School, Boston, MA, August 30, 1995 (received for review May 1, 1995) ABSTRACT CD40 is a 45-kDa glycoprotein member ofthe MATERIALS AND METHODS tumor necrosis factor receptor (TNFR) family expressed on B cells, thymic epithelial cells, dendritic cells, and some carci- Cells. The human B-cell lines Raji, BJAB, and Ramos and the human bladder carcinoma cell line T24 were obtained from noma cells. The unique capacity of CD40 to trigger immuno- American Type Culture Collection. The human B-cell line globulin isotype switching is dependent on the activation of Jijoye which expresses TNFR p80 (CD120b) was a kind gift protein-tyrosine kinases, yet CD40 possesses no kinase do- from G. Mosialos and E. Kieff (Harvard Medical School). main and no known consensus sequences for binding to Human tonsil B cells were purified as described (13). protein-tyrosine kinases. Recently, an intracellular protein Monoclonal Antibodies (mAbs) and Reagents. Mouse anti- (CD40bp/LAP-1/CRAF-1) which belongs to the family of human CD40 mAb 626.1 (IgGl) was a gift from S. M. Fu TNFR-associated proteins was reported to associate with (University of Virginia, Richmond). Murine anti-major histo- CD40. We describe a 23-kDa cell surface protein (p23) which compatibility complex (MHC) class I mAb W6/32 (IgGl), and is specifically associated with CD40 on B cells and on urinary anti-HLA-DR mAb L243 (IgG2a) were obtained through bladder transitional carcinoma cells. -
B Cells +CD5 + CD23 Acute and Chronic Lymphocytic Leukemia
CXC Chemokine Ligand 13 and CC Chemokine Ligand 19 Cooperatively Render Resistance to Apoptosis in B Cell Lineage Acute and Chronic Lymphocytic Leukemia This information is current as CD23+CD5+ B Cells of September 28, 2021. Hu Chunsong, He Yuling, Wang Li, Xiong Jie, Zhou Gang, Zhang Qiuping, Gao Qingping, Zhang Kejian, Qiao Li, Alfred E. Chang, Jin Youxin and Tan Jinquan J Immunol 2006; 177:6713-6722; ; Downloaded from doi: 10.4049/jimmunol.177.10.6713 http://www.jimmunol.org/content/177/10/6713 http://www.jimmunol.org/ References This article cites 54 articles, 31 of which you can access for free at: http://www.jimmunol.org/content/177/10/6713.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 28, 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 © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology CXC Chemokine Ligand 13 and CC Chemokine Ligand 19 Cooperatively Render Resistance to Apoptosis in B Cell Lineage Acute and Chronic Lymphocytic Leukemia CD23؉CD5؉ B Cells1 Hu Chunsong,2*† He Yuling,2† Wang Li,2† Xiong Jie,†‡ Zhou Gang,† Zhang Qiuping,† Gao Qingping,§ Zhang Kejian,§ Qiao Li,†¶ Alfred E.