Flow Cytometric Characterization of CD71 Cell Subsets In

Total Page:16

File Type:pdf, Size:1020Kb

Flow Cytometric Characterization of CD71 Cell Subsets In Leukemia (2000) 14, 816–825 2000 Macmillan Publishers Ltd All rights reserved 0887-6924/00 $15.00 www.nature.com/leu BIOMED-1 Concerted Action report: Flow cytometric characterization of CD71 cell subsets in normal bone marrow as a basis for the diagnosis and follow-up of T cell acute lymphoblastic leukemia (T-ALL) A Porwit-MacDonald1, E Bjo¨rklund1, P Lucio2, EG van Lochem3, J Mazur1, A Parreira2, MWM van den Beemd3, ER van Wering4, E Baars4, G Gaipa5, A Biondi5, J Ciudad6, JJM van Dongen3, JF San Miguel6 and A Orfao6 1Department of Pathology, Karolinska Hospital, Stockholm, Sweden; 2Instituto Portugues de Oncologia, Lisboa, Portugal; 3Department of Immunology, Erasmus University, Rotterdam, and University Hospital, Rotterdam, The Netherlands; 4Dutch Childhood Leukemia Study Group, The Hague, The Netherlands; 5Centro di Ricerca M Tettamanti, Monza, Italy; and 6Department of Hematology, University Hospital, Salamanca, Spain The European BIOMED-1 Concerted Action was initiated in multiparameter flow cytometry for the investigation of MRD 1994 to improve and standardize the flow cytometric detection can reach a high sensitivity and specificity for the identifi- of minimal residual disease (MRD) in acute leukemia (AL). 8–11 Three different protocols were defined to identify the normal cation of residual leukemic T lymphoblasts. A cooperative subsets of B, T and myeloid cells in bone marrow (BM), and study conducted by six European centers involved in the were applied to the different types of AL in order to study BIOMED-1 Concerted Action ‘Investigation of Minimal aberrant immunophenotypes. Using sensitive acquisition Residual Disease in Acute Leukemia: International Standardiz- methods (‘live gate’) T cell subsets in normal BM could be ation and Clinical Evaluation’ applied multiparameter flow identified with five triple-stains: CD7/CD5/CD3, CD7/CD4/CD8, cytometry in which triple antibody combinations were used CD7/CD2/CD3, CD7/CD38/CD34 and TdT/CD7/surface or cyto- plasmic (cy)CD3 (antibodies conjugated with FITC/PE/PECy5 or together with sensitive data acquisition methods (such as ‘live PerCP, respectively). The identification of T cell subsets in BM gate’ acquisition). Using this approach we obtained detailed allowed definition of ‘empty spaces’ (ie areas of flow cytometric information on cell subsets that are present in normal BM at plots where normally no cells are found). All studied T-ALL very low frequencies and that may remain undetected using cases (n = 65) were located in ‘empty spaces’ and could be conventional methods of analysis. discriminated from normal T cells. The most informative triple The immunophenotyping methods (staining protocols and staining was TdT/CD7/cyCD3, which was aberrant in 91% of T- ALL cases. In most cases, two or more aberrant patterns were flow cytometry) were carefully standardized in order to found. Apparently the immunophenotypes of T-ALL differ sig- develop a highly reproducible and sensitive approach to nificantly from normal BM T cells. This is mostly caused by identify both major and minor subsets of T cells present in BM their thymocytic origin, but also the neoplastic transformation and their relative distribution according to age. Once normal might have affected antigen expression patterns. Application T cell subsets were identified, we focused our attention on of the five proposed marker combinations in T-ALL contributes the ‘empty spaces’ left in multidimensional flow cytometry dot to standardized detection of MRD, since cells persistent or plots of each studied antigen combination, as has previously reappearing in the ‘empty spaces’ can be easily identified in 12–14 follow-up BM samples during and after treatment. Leukemia been reported for precursor B cells. Subsequently, we (2000) 14, 816–825. used the same triple antibody combinations and flow cytome- Keywords: T cells; bone marrow; acute lymphoblastic leukemia; try protocols to analyze 65 consecutive T-ALL cases diag- immunophenotype; flow cytometry; minimal residual disease nosed in the six participating laboratories. Our aim was to assess the incidence of aberrant phenotypes, which can be used for the follow-up of MRD in T-ALL patients. Introduction It has long been assumed that blasts from T cell acute lym- Materials and methods phoblastic leukemia (T-ALL) reflect the immunophenotypes of early stages of T cell differentiation.1–3 Most T-ALL cases dis- Specimen collection play phenotypes corresponding to various stages of thymocyte differentiation, which normally are not found in bone marrow (BM) or peripheral blood (PB).4 Normal BM samples: Normal BM samples (n = 35) were The aberrant immunophenotypic characteristics of leu- obtained from healthy donors (n = 29) and patients with idio- kemic T lymphoblasts allow discrimination from T cell subsets pathic thrombocytopenia (ITP) (n = 6), recruited in the six Eur- in BM and thus can be used for detection of minimal residual opean centers involved in the BIOMED-1 Concerted Action disease (MRD).5–8 A comprehensive analysis of the immuno- on MRD. The following centers participated: Portuguese Insti- phenotypic characteristics of T cells and the subsequent tute of Oncology, Lisbon, Portugal; Karolinska Hospital, identification of all T cell subsets in normal BM are important Stockholm, Sweden; University of Salamanca, Salamanca, for the reliable distinction between normal and leukemic T Spain; Department of Immunology, Erasmus University, Rot- cells. terdam and University Hospital, Rotterdam, The Netherlands; Previous studies in T-ALL strongly suggest that the use of Dutch Childhood Leukemia Study Group, The Hague, The Netherlands; and M Tettamanti Research Center, Monza, Italy. Informed consent was obtained from all donors or parents Correspondence: A Porwit-MacDonald, Department of Pathology, in cases of children less than 15 years old in accordance with Karolinska Hospital, 171 76 Stockholm, Sweden; Fax: 46 851775843 J Mazur was on leave from Department of Epidemiology and Health local Medical Ethics Committees. The samples from patients Care Planning, Institute Mother and Child, Warsaw, Poland with ITP were obtained for diagnostic purposes. The median Received 14 June 1999; accepted 15 December 1999 age of the donors was 15 years, ranging from 2 to 75 years BIOMED-1 Concerted Action report A Porwit-MacDonald et al 817 old (mean age 24), the male/female ratio was 0.8. Moreover, studies showed that both intracellular staining procedures 16 follow-up BM samples from children receiving chemo- yielded similar results.14,15 therapy for B-precursor ALL were included to investigate if T For standardization purposes, we used triple combinations cell content and distribution changed during cytostatic of the same Mab clones labeled with identical fluorochromes treatment. (FITC/PE/PECy5 or PerCP) in all immunostainings of normal BM in all participating centers: CD7/CD5/CD3, CD7/CD4/CD8, CD7/CD2/CD3, CD7/CD38/CD34 and Leukemic samples: T-ALL samples (n = 65) were obtained TdT/CD7/cyCD3 (Table 1). Isotype-matched immunoglobulins in the participating centers for diagnostic purposes. The mor- and a sample stained for CD3-FITC/CD4-PE/CD8-PE/Cy5 were phological diagnosis of ALL was made on the basis of micro- used as negative and positive controls, respectively. Addition- scopic investigation of May–Gru¨nwald-Giemsa stained BM ally, expression of CD13, CD33 and CD19 within the CD7+ smears. The immunologic diagnosis of T-ALL was made cell population was studied in BM samples from a total of 24 according to well-established criteria.4 The median age of the normal donors in Salamanca. The immunostaining of leu- patients was 13 years, ranging from 1 to 52 years (mean 16), kemic samples was performed using the same triple antibody and the male/female ratio was 1.8. combinations and sample preparation procedures as for normal BM. Sample preparation Data acquisition and analysis Bone marrow aspirates were collected in either heparin or EDTA anticoagulant and maintained at room temperature (RT) Data acquisition was performed in all centers in a stan- until processed (not longer than 24 h). The nucleated cell dardized manner, using FACScan flow-cytometers (BD), count was adjusted to 1–2 × 107 cells/ml. For sample prep- equipped with either LysisII or CellQuest (BD) software pro- aration, a stain and then lyse/wash technique was used. grams. Instrument set-up and calibration was performed in a Briefly, 100 µl of BM cell suspension (at least 1 × 106 standardized way as previously described.12 For the analysis nucleated cells) were incubated for 10–15 min (RT, in the of normal BM samples, a two-step acquisition procedure was dark) with saturating amounts of five different triple combi- used. First, 15 × 103 non-gated events were acquired from the nations of monoclonal antibodies (Mab, Table 1). After incu- BM samples. Then a total of 105 to 2 × 106 cells were meas- bation, 2 ml of FACS lysing solution (Becton Dickinson (BD), ured with a live gate set on the basis of CD7 expression and San Jose, CA, USA) diluted 1/10 in distilled water was added low/intermediate side scatter (SSC) characteristics. In this and samples were incubated for another 10 min at RT in the second step, data acquisition exclusively concerned CD7+ dark. Subsequently, cells were washed and re-suspended in 1 cells with lymphoid scatter generally representing approxi- ml of PBS. mately 10% of BM cells (Table 2). In practice, this meant that Cytoplasmic (cy)CD3 and nuclear terminal deoxynucleoti- between 5 × 104 and 2 × 105 CD7+ lymphoid BM cells were dyl transferase (TdT) were detected after staining for surface acquired for further evaluation. The expression of the other T markers (as above), and fixation/permeabilization with Perme- cell markers was analyzed within this CD7+ lymphocyte gate afix (OPM; Ortho, Raritan, NY, USA) or Fix & Perm (F/P; An in order to characterize the different CD7+ cell subsets. der Grub, Vienna, Austria).15 The reagents were used follow- Additional live gates were based on CD34+ and TdT+ events ing the manufacturer’s recommendations.
Recommended publications
  • And Heterodimeric Interactions Between the Gene Products of PKD1 and PKD2 (Polycystic Kidney Disease͞yeast Two-Hybrid System͞protein–Protein Interactions)
    Proc. Natl. Acad. Sci. USA Vol. 94, pp. 6965–6970, June 1997 Medical Sciences Homo- and heterodimeric interactions between the gene products of PKD1 and PKD2 (polycystic kidney diseaseyyeast two-hybrid systemyprotein–protein interactions) LEONIDAS TSIOKAS*†,EMILY KIM†‡,THIERRY ARNOULD*, VIKAS P. SUKHATME*, AND GERD WALZ*§ *Renal Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215; and ‡Laboratory of Molecular and Developmental Neuroscience, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114 Communicated by Irving M. London, Massachusetts Institute of Technology, Cambridge, MA, May 1, 1997 (received for review January 3, 1997) ABSTRACT PKD1 and PKD2 are two recently identified clarified the nature of the aberrant gene products caused by genes that are responsible for the vast majority of autosomal mutations of PKD1 and PKD2. Renal cysts are thought to arise polycystic kidney disease, a common inherited disease that through a process of persistent epithelial proliferation related causes progressive renal failure. PKD1 encodes polycystin, a to the lack of terminal differentiation. Both abnormal growth large glycoprotein that contains several extracellular motifs factor responsiveness (8–12) and the elevated expression of indicative of a role in cell–cell or cell–matrix interactions, and certain oncogenes appear to support this hypothesis (13–16). the PKD2 encodes a protein with homology to a voltage- Recently, loss of heterozygosity was discovered within a subset activated calcium channel and to PKD1. It is currently un- of cysts for two closely linked polymorphic markers located known how mutations of either protein functionally cause within the PKD1 gene, indicating that cyst formation in autosomal polycystic kidney disease.
    [Show full text]
  • 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.
    [Show full text]
  • 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,
    [Show full text]
  • CD29 Identifies IFN-Γ–Producing Human CD8+ T Cells With
    + CD29 identifies IFN-γ–producing human CD8 T cells with an increased cytotoxic potential Benoît P. Nicoleta,b, Aurélie Guislaina,b, Floris P. J. van Alphenc, Raquel Gomez-Eerlandd, Ton N. M. Schumacherd, Maartje van den Biggelaarc,e, and Monika C. Wolkersa,b,1 aDepartment of Hematopoiesis, Sanquin Research, 1066 CX Amsterdam, The Netherlands; bLandsteiner Laboratory, Oncode Institute, Amsterdam University Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; cDepartment of Research Facilities, Sanquin Research, 1066 CX Amsterdam, The Netherlands; dDivision of Molecular Oncology and Immunology, Oncode Institute, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands; and eDepartment of Molecular and Cellular Haemostasis, Sanquin Research, 1066 CX Amsterdam, The Netherlands Edited by Anjana Rao, La Jolla Institute for Allergy and Immunology, La Jolla, CA, and approved February 12, 2020 (received for review August 12, 2019) Cytotoxic CD8+ T cells can effectively kill target cells by producing therefore developed a protocol that allowed for efficient iso- cytokines, chemokines, and granzymes. Expression of these effector lation of RNA and protein from fluorescence-activated cell molecules is however highly divergent, and tools that identify and sorting (FACS)-sorted fixed T cells after intracellular cytokine + preselect CD8 T cells with a cytotoxic expression profile are lacking. staining. With this top-down approach, we performed an un- + Human CD8 T cells can be divided into IFN-γ– and IL-2–producing biased RNA-sequencing (RNA-seq) and mass spectrometry cells. Unbiased transcriptomics and proteomics analysis on cytokine- γ– – + + (MS) analyses on IFN- and IL-2 producing primary human producing fixed CD8 T cells revealed that IL-2 cells produce helper + + + CD8 Tcells.
    [Show full text]
  • Expression of Endothelial Cell-Associated Molecules in AML
    Leukemia (2002) 16, 112–119 2002 Nature Publishing Group All rights reserved 0887-6924/02 $25.00 www.nature.com/leu Expression of endothelial cell-associated molecules in AML cells M Watarai1, H Miwa1, M Shikami1, K Sugamura1, M Wakabayashi1, A Satoh1, K Tsuboi1, A Imamura1, H Mihara1, Y Katoh1, K Kita2 and M Nitta1 1Department of Internal Medicine, Division of Hematology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan; and 2Tokura Hospital, Uji, Kyoto, Japan Recently, it has been clarified that interaction between hemato- hematopoietic cells is also mediated by adhesion molecules poietic cells and endothelial cells is important in normal hema- such as integrins, as well as soluble factors.10,11 topoiesis and leukemogenesis. In this study, we examined the relationship between AML cells and endothelial cells by analyz- Angiopoietins and VEGF are recognized to act coordinately ing the expression profile of angiogenic factors, angiopoietin- during vascular growth and remodeling. Blood vessels remain 1 (Ang-1), Ang-2, Tie-2 (a receptor for angiopoietins) and vascu- in a stable state when Tie-2 receptor is constitutively engaged lar endothelial growth factor (VEGF). Our results demonstrated with angiopoietin-1 (Ang-1) by stabilizing blood vessels -that CD7(؉)AML expressed Ang-2 mRNA frequently and inte- through interactions with perivascular cells and the extracellu grin-family adhesion molecules (CD11c and CD18) intensively, lar matrix. When Ang-2 expression is up-regulated, the inter- suggesting the close correlation with endothelial cells. On the other hand, in t(8;21) AML cells, expression of Ang-2 was action between Tie-2 and Ang-1 is disrupted, and the vessel infrequent and expression of integrin-family adhesion mol- is destabilized.
    [Show full text]
  • Cx3cr1 Mediates the Development of Monocyte-Derived Dendritic Cells During Hepatic Inflammation
    CX3CR1 MEDIATES THE DEVELOPMENT OF MONOCYTE-DERIVED DENDRITIC CELLS DURING HEPATIC INFLAMMATION. Supplementary material Supplementary Figure 1: Liver CD45+ myeloid cells were pre-gated for Ly6G negative cells for excluding granulocytes and HDCs subsequently analyzed among the cells that were CD11c+ and had high expression of MHCII. Supplementary Table 1 low/- high + Changes in gene expression between CX3CR1 and CX3CR1 CD11b myeloid hepatic dendritic cells (HDCs) from CCl4-treated mice high Genes up-regulated in CX3CR1 HDCs Gene Fold changes P value Full name App 4,01702 5,89E-05 amyloid beta (A4) precursor protein C1qa 9,75881 1,69E-22 complement component 1, q subcomponent, alpha polypeptide C1qb 9,19882 3,62E-20 complement component 1, q subcomponent, beta polypeptide Ccl12 2,51899 0,011769 chemokine (C-C motif) ligand 12 Ccl2 6,53486 6,37E-11 chemokine (C-C motif) ligand 2 Ccl3 4,99649 5,84E-07 chemokine (C-C motif) ligand 3 Ccl4 4,42552 9,62E-06 chemokine (C-C motif) ligand 4 Ccl6 3,9311 8,46E-05 chemokine (C-C motif) ligand 6 Ccl7 2,60184 0,009272 chemokine (C-C motif) ligand 7 Ccl9 4,17294 3,01E-05 chemokine (C-C motif) ligand 9 Ccr2 3,35195 0,000802 chemokine (C-C motif) receptor 2 Ccr5 3,23358 0,001222 chemokine (C-C motif) receptor 5 Cd14 6,13325 8,61E-10 CD14 antigen Cd36 2,94367 0,003243 CD36 antigen Cd44 4,89958 9,60E-07 CD44 antigen Cd81 6,49623 8,24E-11 CD81 antigen Cd9 3,06253 0,002195 CD9 antigen Cdkn1a 4,65279 3,27E-06 cyclin-dependent kinase inhibitor 1A (P21) Cebpb 6,6083 3,89E-11 CCAAT/enhancer binding protein (C/EBP),
    [Show full text]
  • Molecular Signatures Differentiate Immune States in Type 1 Diabetes Families
    Page 1 of 65 Diabetes Molecular signatures differentiate immune states in Type 1 diabetes families Yi-Guang Chen1, Susanne M. Cabrera1, Shuang Jia1, Mary L. Kaldunski1, Joanna Kramer1, Sami Cheong2, Rhonda Geoffrey1, Mark F. Roethle1, Jeffrey E. Woodliff3, Carla J. Greenbaum4, Xujing Wang5, and Martin J. Hessner1 1The Max McGee National Research Center for Juvenile Diabetes, Children's Research Institute of Children's Hospital of Wisconsin, and Department of Pediatrics at the Medical College of Wisconsin Milwaukee, WI 53226, USA. 2The Department of Mathematical Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI 53211, USA. 3Flow Cytometry & Cell Separation Facility, Bindley Bioscience Center, Purdue University, West Lafayette, IN 47907, USA. 4Diabetes Research Program, Benaroya Research Institute, Seattle, WA, 98101, USA. 5Systems Biology Center, the National Heart, Lung, and Blood Institute, the National Institutes of Health, Bethesda, MD 20824, USA. Corresponding author: Martin J. Hessner, Ph.D., The Department of Pediatrics, The Medical College of Wisconsin, Milwaukee, WI 53226, USA Tel: 011-1-414-955-4496; Fax: 011-1-414-955-6663; E-mail: [email protected]. Running title: Innate Inflammation in T1D Families Word count: 3999 Number of Tables: 1 Number of Figures: 7 1 For Peer Review Only Diabetes Publish Ahead of Print, published online April 23, 2014 Diabetes Page 2 of 65 ABSTRACT Mechanisms associated with Type 1 diabetes (T1D) development remain incompletely defined. Employing a sensitive array-based bioassay where patient plasma is used to induce transcriptional responses in healthy leukocytes, we previously reported disease-specific, partially IL-1 dependent, signatures associated with pre and recent onset (RO) T1D relative to unrelated healthy controls (uHC).
    [Show full text]
  • Subsets Identifies Multiple CD8 T Cell Effector CD7 Is a Differentiation
    CD7 Is a Differentiation Marker That Identifies Multiple CD8 T Cell Effector Subsets This information is current as Einar M. Aandahl, Johan K. Sandberg, Karen P. Beckerman, of September 29, 2021. Kjetil Taskén, Walter J. Moretto and Douglas F. Nixon J Immunol 2003; 170:2349-2355; ; doi: 10.4049/jimmunol.170.5.2349 http://www.jimmunol.org/content/170/5/2349 Downloaded from References This article cites 44 articles, 22 of which you can access for free at: http://www.jimmunol.org/content/170/5/2349.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 29, 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 © 2003 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology CD7 Is a Differentiation Marker That Identifies Multiple CD8 T Cell Effector Subsets1 Einar M. Aandahl,2* Johan K. Sandberg,* Karen P. Beckerman,* Kjetil Taske´n,† Walter J. Moretto,* and Douglas F.
    [Show full text]
  • Human CD Marker Chart Reviewed by HLDA1 Bdbiosciences.Com/Cdmarkers
    BD Biosciences Human CD Marker Chart Reviewed by HLDA1 bdbiosciences.com/cdmarkers 23-12399-01 CD Alternative Name Ligands & Associated Molecules T Cell B Cell Dendritic Cell NK Cell Stem Cell/Precursor Macrophage/Monocyte Granulocyte Platelet Erythrocyte Endothelial Cell Epithelial Cell CD Alternative Name Ligands & Associated Molecules T Cell B Cell Dendritic Cell NK Cell Stem Cell/Precursor Macrophage/Monocyte Granulocyte Platelet Erythrocyte Endothelial Cell Epithelial Cell CD Alternative Name Ligands & Associated Molecules T Cell B Cell Dendritic Cell NK Cell Stem Cell/Precursor Macrophage/Monocyte Granulocyte Platelet Erythrocyte Endothelial Cell Epithelial Cell CD1a R4, T6, Leu6, HTA1 b-2-Microglobulin, CD74 + + + – + – – – CD93 C1QR1,C1qRP, MXRA4, C1qR(P), Dj737e23.1, GR11 – – – – – + + – – + – CD220 Insulin receptor (INSR), IR Insulin, IGF-2 + + + + + + + + + Insulin-like growth factor 1 receptor (IGF1R), IGF-1R, type I IGF receptor (IGF-IR), CD1b R1, T6m Leu6 b-2-Microglobulin + + + – + – – – CD94 KLRD1, Kp43 HLA class I, NKG2-A, p39 + – + – – – – – – CD221 Insulin-like growth factor 1 (IGF-I), IGF-II, Insulin JTK13 + + + + + + + + + CD1c M241, R7, T6, Leu6, BDCA1 b-2-Microglobulin + + + – + – – – CD178, FASLG, APO-1, FAS, TNFRSF6, CD95L, APT1LG1, APT1, FAS1, FASTM, CD95 CD178 (Fas ligand) + + + + + – – IGF-II, TGF-b latency-associated peptide (LAP), Proliferin, Prorenin, Plasminogen, ALPS1A, TNFSF6, FASL Cation-independent mannose-6-phosphate receptor (M6P-R, CIM6PR, CIMPR, CI- CD1d R3G1, R3 b-2-Microglobulin, MHC II CD222 Leukemia
    [Show full text]
  • 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.
    [Show full text]
  • CD5-Positive Acute Lymphoblastic Leukemia Dawood Ahmed1, Tahir Aziz Ahmed1, Suhaib Ahmed 2, Hamid Nawaz Tipu1 and Muhammad Amin Wiqar1
    CASE REPORT CD5-Positive Acute Lymphoblastic Leukemia Dawood Ahmed1, Tahir Aziz Ahmed1, Suhaib Ahmed 2, Hamid Nawaz Tipu1 and Muhammad Amin Wiqar1 ABSTRACT CD5-positive B-ALL is a rare variant of Acute Lymphoblastic Leukemia (ALL). In literature, only three cases have been reported so far. This fourth case report describes a young lady who was diagnosed as ALL (L-2) on bone marrow examination and was found to be CD5 positive B-cell acute lymphoblastic leukemia on immunophenotyping. Cytogenetic analysis revealed translocation t(9:22). Key words: CD5. Immunophenotyping. Acute lymphoblastic leukemia. INTRODUCTION blood examination. On peripheral blood examination hemoglobin (Hb) was reported 7.6 g/dl, Total Leukocyte CD5 is a 67-kd glycoprotein that is expressed by most Count (TLC) 18,600/µl with 85% lymphocytes, 9% T-cells and a subset of B-cells called B-1 cells. neutrophils, 4% eosinophils and 2% monocytes. CD5-positive B-cells are found in fetal spleen, cord Lymphocytes were described as atypical and abnormal blood and peritoneal cavity of adults. Similar cells are cells and bone marrow aspiration was advised. Blood also present in the marginal zones of lymphoid follicles counts carried out at the time of bone marrow aspiration in spleen. Only 5 to 10% of B-cells belong to this revealed ESR 120 mm after one hour, Hb 5.3 g/dl, TLC category in blood and lymphoid tissues.1 These cells 26,900/µl with 82% lymphocytes and 18% neutrophils in produce IgM antibodies (natural antibodies) against the peripheral blood specimen. Platelets count was polysaccharide and lipid antigens.
    [Show full text]
  • Mouse CD Marker Chart Bdbiosciences.Com/Cdmarkers
    BD Mouse CD Marker Chart bdbiosciences.com/cdmarkers 23-12400-01 CD Alternative Name Ligands & Associated Molecules T Cell B Cell Dendritic Cell NK Cell Stem Cell/Precursor Macrophage/Monocyte Granulocyte Platelet Erythrocyte Endothelial Cell Epithelial Cell CD Alternative Name Ligands & Associated Molecules T Cell B Cell Dendritic Cell NK Cell Stem Cell/Precursor Macrophage/Monocyte Granulocyte Platelet Erythrocyte Endothelial Cell Epithelial Cell CD Alternative Name Ligands & Associated Molecules T Cell B Cell Dendritic Cell NK Cell Stem Cell/Precursor Macrophage/Monocyte Granulocyte Platelet Erythrocyte Endothelial Cell Epithelial Cell CD1d CD1.1, CD1.2, Ly-38 Lipid, Glycolipid Ag + + + + + + + + CD104 Integrin b4 Laminin, Plectin + DNAX accessory molecule 1 (DNAM-1), Platelet and T cell CD226 activation antigen 1 (PTA-1), T lineage-specific activation antigen 1 CD112, CD155, LFA-1 + + + + + – + – – CD2 LFA-2, Ly-37, Ly37 CD48, CD58, CD59, CD15 + + + + + CD105 Endoglin TGF-b + + antigen (TLiSA1) Mucin 1 (MUC1, MUC-1), DF3 antigen, H23 antigen, PUM, PEM, CD227 CD54, CD169, Selectins; Grb2, β-Catenin, GSK-3β CD3g CD3g, CD3 g chain, T3g TCR complex + CD106 VCAM-1 VLA-4 + + EMA, Tumor-associated mucin, Episialin + + + + + + Melanotransferrin (MT, MTF1), p97 Melanoma antigen CD3d CD3d, CD3 d chain, T3d TCR complex + CD107a LAMP-1 Collagen, Laminin, Fibronectin + + + CD228 Iron, Plasminogen, pro-UPA (p97, MAP97), Mfi2, gp95 + + CD3e CD3e, CD3 e chain, CD3, T3e TCR complex + + CD107b LAMP-2, LGP-96, LAMP-B + + Lymphocyte antigen 9 (Ly9),
    [Show full text]