Adenovirus Species B Interactions with CD46
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(CD147) Is Induced by C/Ebpβ and Is Differentially Expressed in ALK+
Laboratory Investigation (2017) 97, 1095–1102 © 2017 USCAP, Inc All rights reserved 0023-6837/17 EMMPRIN (CD147) is induced by C/EBPβ and is differentially expressed in ALK+ and ALK − anaplastic large-cell lymphoma Janine Schmidt1, Irina Bonzheim1, Julia Steinhilber1, Ivonne A Montes-Mojarro1, Carlos Ortiz-Hidalgo2, Wolfram Klapper3, Falko Fend1 and Leticia Quintanilla-Martínez1 Anaplastic lymphoma kinase-positive (ALK+) anaplastic large-cell lymphoma (ALCL) is characterized by expression of oncogenic ALK fusion proteins due to the translocation t(2;5)(p23;q35) or variants. Although genotypically a T-cell lymphoma, ALK+ ALCL cells frequently show loss of T-cell-specific surface antigens and expression of monocytic markers. C/EBPβ, a transcription factor constitutively overexpressed in ALK+ ALCL cells, has been shown to play an important role in the activation and differentiation of macrophages and is furthermore capable of transdifferentiating B-cell and T-cell progenitors to macrophages in vitro. To analyze the role of C/EBPβ for the unusual phenotype of ALK+ ALCL cells, C/EBPβ was knocked down by RNA interference in two ALK+ ALCL cell lines, and surface antigen expression profiles of these cell lines were generated using a Human Cell Surface Marker Screening Panel (BD Biosciences). Interesting candidate antigens were further analyzed by immunohistochemistry in primary ALCL ALK+ and ALK − cases. Antigen expression profiling revealed marked changes in the expression of the activation markers CD25, CD30, CD98, CD147, and CD227 after C/EBPβ knockdown. Immunohistochemical analysis confirmed a strong, membranous CD147 (EMMPRIN) expression in ALK+ ALCL cases. In contrast, ALK − ALCL cases showed a weaker CD147 expression. -
CD46 Expression Is Indicative of Shorter Revival-Free Survival for Ovarian Cancer Patients
ANTICANCER RESEARCH 26: 4943-4948 (2006) CD46 Expression is Indicative of Shorter Revival-free Survival for Ovarian Cancer Patients PAWEL SUROWIAK1,2,3, VERENA MATERNA1, ADAM MACIEJCZYK3, IRINA KAPLENKO4, MAREK SPACZYNSKI4, MANFRED DIETEL1, HERMANN LAGE1 and MACIEJ ZABEL2,5 1Institute of Pathology, Charité Campus Mitte, D-10117 Berlin, Germany; 2Chair and Department of Histology and Embryology, University School of Medicine, ul. Chalubinskiego 6a, 50-356 Wroclaw; 3Lower Silesian Centre of Oncology, pl. Hirszfelda 12, 53-413 Wroclaw; 4Chair and Department of Obstetrics and Gynaecology and 5Chair and Department of Histology and Embryology, University School of Medicine, ul. Swiecickiego 6, 60-781 Poznan, Poland Abstract. Background: The membrane cofactor protein CD46 cure very rarely. Despite the introduction of novel represents a complement inhibitor, which protects autologous chemotherapy regimens, the frequency of 5 - year survival cells from complement - mediated cytotoxicity. CD46 may of patients at all clinical stages has not exceeded 40%, in the exhibit the potential to protect tumor cells from the immune last 20 years (2). Therefore, intense efforts are being made responses of the host. The present study aimed to evaluate the in numerous centres to detect new prognostic factors, which prognostic significance of CD46 expression in ovarian cancers. might prove valuable towards studies on new therapeutic Materials and Methods: The analyses were performed on 73 approaches. ovarian cancer samples. Immunohistochemical reactions were The absence of the host’s immune response to the performed on paraffin sections of tumors using monoclonal presence of tumor cells represents one of the circumstances, antibodies directed against CD46. The immunohistochemical which promotes development of the tumor. -
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. -
The Membrane Complement Regulatory Protein CD59 and Its Association with Rheumatoid Arthritis and Systemic Lupus Erythematosus
Current Medicine Research and Practice 9 (2019) 182e188 Contents lists available at ScienceDirect Current Medicine Research and Practice journal homepage: www.elsevier.com/locate/cmrp Review Article The membrane complement regulatory protein CD59 and its association with rheumatoid arthritis and systemic lupus erythematosus * Nibhriti Das a, Devyani Anand a, Bintili Biswas b, Deepa Kumari c, Monika Gandhi c, a Department of Biochemistry, All India Institute of Medical Sciences, New Delhi 110029, India b Department of Zoology, Ramjas College, University of Delhi, India c University School of Biotechnology, Guru Gobind Singh Indraprastha University, India article info abstract Article history: The complement cascade consisting of about 50 soluble and cell surface proteins is activated in auto- Received 8 May 2019 immune inflammatory disorders. This contributes to the pathological manifestations in these diseases. In Accepted 30 July 2019 normal health, the soluble and membrane complement regulatory proteins protect the host against Available online 5 August 2019 complement-mediated self-tissue injury by controlling the extent of complement activation within the desired limits for the host's benefit. CD59 is a membrane complement regulatory protein that inhibits the Keywords: formation of the terminal complement complex or membrane attack complex (C5b6789n) which is CD59 generated on complement activation by any of the three pathways, namely, the classical, alternative, and RA SLE the mannose-binding lectin pathway. Animal experiments and human studies have suggested impor- Pathophysiology tance of membrane complement proteins including CD59 in the pathophysiology of rheumatoid arthritis Disease marker (RA) and systemic lupus erythematosus (SLE). Here is a brief review on CD59 and its distribution, structure, functions, and association with RA and SLE starting with a brief introduction on the com- plement system, its activation, the biological functions, and relations of membrane complement regu- latory proteins, especially CD59, with RA and SLE. -
More Than a Pore: Nonlytic Antimicrobial Functions of Downloaded from Complement and Bacterial Strategies for Evasion
REVIEW More than a Pore: Nonlytic Antimicrobial Functions of Downloaded from Complement and Bacterial Strategies for Evasion Elisabet Bjanes,a Victor Nizeta,b aDivision of Host-Microbe Systems and Therapeutics, Department of Pediatrics, UC San Diego, La Jolla, California, USA bSkaggs School of Pharmacy and Pharmaceutical Sciences, UC San Diego, La Jolla, California, USA http://mmbr.asm.org/ SUMMARY ........................................................................1 INTRODUCTION ...................................................................2 BY THE BOOK: CANONICAL COMPLEMENT CASCADES ...............................2 Off to the Races—Pathway Activation . 2 More and More—Amplification . 3 End of the Line—Termination . 3 Pump the Brakes—Inhibition . 5 Surviving MAC Attack—Evasion of Complement Lysis by Gram-Negative Bacteria . 6 NONLYTIC COMPLEMENT FUNCTIONS AND BACTERIAL EVASION MECHANISMS ......8 Special Considerations in Gram-Positive Bacteria . 8 on January 27, 2021 at UNIV OF CALIF SAN DIEGO Preparing the Meal—Complement Aids Opsonization and Phagocytosis . 8 Food for Thought—Complement Traffics to Autophagy . 10 Fueling the Fire—Complement Modulates Inflammatory Responses . 11 Casting a Wider NET—Complement and Neutrophil Synergy . 12 Inside Scoop—Novel Roles of Intracellular Complement . 13 Tying the Clot—Complement and Coagulation Cross Talk . 15 Bridging the Gap—Complement Instructs Adaptive Immunity . 17 REFRAMING SCIENTIFIC PARADIGMS AND THERAPEUTIC APPROACHES TO ENCOMPASS COMPLEMENT ..................................................18 -
B-Cell Receptor Pathway Inhibitors Affect CD20 Levels and Impair Antitumor Activity of Anti-CD20 Monoclonal Antibodies
Letters to the Editor 1163 13 Kuruvilla J, Gutierrez M, Shah BD, Gabrail NY, de Nully Brown P, 14 Yu L, Mohamed AJ, Simonson OE, Vargas L, Blomberg KE, Bjorkstrand B et al. Stone RM et al. Preliminary evidence of anti tumor activity of selinexor Proteasome-dependent autoregulation of Bruton tyrosine kinase (Btk) promoter (KPT-330) in a phase I trial of a first-in-class oral selective inhibitor via NF-kappaB. Blood 2008; 111: 4617–4626. of nuclear export (SINE) in patients (pts) with relapsed/refractory non 15BurgerJA,BurgerM,KippsTJ.Chronic lymphocytic leukemia B cells Hodgkin’s lymphoma (NHL) and chronic lymphocytic leukemia (CLL). Blood 2013; express functional CXCR4 chemokine receptors that mediate spontaneous 122: 90. migration beneath bone marrow stromal cells. Blood 1999; 94: 3658–3667. Supplementary Information accompanies this paper on the Leukemia website (http://www.nature.com/leu) B-cell receptor pathway inhibitors affect CD20 levels and impair antitumor activity of anti-CD20 monoclonal antibodies Leukemia (2014) 28, 1163–1167; doi:10.1038/leu.2014.12 also tested a primary MCL sample and upon treatment with BCR inhibitors observed a significant downregulation of surface CD20 levels and a trend towards impaired R-CDC and O-CDC (Supplementary Figure 1b). Moreover, we determined the Signaling via the aberrantly activated B-cell receptor (BCR) has a influence of BCR inhibitors on CD20 surface levels in a critical role in the pathogenesis of B-cell tumors by promoting series of 15 tumor cell lines, including Burkitt’s lymphoma (Ramos, survival and clonal expansion of malignant B cells.1,2 Multiple Daudi and BJAB), ALL (NALM-6), diffuse large B-cell lymphoma preclinical studies indicate that blocking various components of (BCR-dependent Ly-1, Ly-7, Ly-10, DHL-6, HBL-1, U2932 and the BCR signaling pathway holds a great therapeutic potential in BCR-independent Ly-4, Ly-19, Pfeiffer) and CLL (EHEB and MEC-1). -
Single-Cell RNA Sequencing Demonstrates the Molecular and Cellular Reprogramming of Metastatic Lung Adenocarcinoma
ARTICLE https://doi.org/10.1038/s41467-020-16164-1 OPEN Single-cell RNA sequencing demonstrates the molecular and cellular reprogramming of metastatic lung adenocarcinoma Nayoung Kim 1,2,3,13, Hong Kwan Kim4,13, Kyungjong Lee 5,13, Yourae Hong 1,6, Jong Ho Cho4, Jung Won Choi7, Jung-Il Lee7, Yeon-Lim Suh8,BoMiKu9, Hye Hyeon Eum 1,2,3, Soyean Choi 1, Yoon-La Choi6,10,11, Je-Gun Joung1, Woong-Yang Park 1,2,6, Hyun Ae Jung12, Jong-Mu Sun12, Se-Hoon Lee12, ✉ ✉ Jin Seok Ahn12, Keunchil Park12, Myung-Ju Ahn 12 & Hae-Ock Lee 1,2,3,6 1234567890():,; Advanced metastatic cancer poses utmost clinical challenges and may present molecular and cellular features distinct from an early-stage cancer. Herein, we present single-cell tran- scriptome profiling of metastatic lung adenocarcinoma, the most prevalent histological lung cancer type diagnosed at stage IV in over 40% of all cases. From 208,506 cells populating the normal tissues or early to metastatic stage cancer in 44 patients, we identify a cancer cell subtype deviating from the normal differentiation trajectory and dominating the metastatic stage. In all stages, the stromal and immune cell dynamics reveal ontological and functional changes that create a pro-tumoral and immunosuppressive microenvironment. Normal resident myeloid cell populations are gradually replaced with monocyte-derived macrophages and dendritic cells, along with T-cell exhaustion. This extensive single-cell analysis enhances our understanding of molecular and cellular dynamics in metastatic lung cancer and reveals potential diagnostic and therapeutic targets in cancer-microenvironment interactions. 1 Samsung Genome Institute, Samsung Medical Center, Seoul 06351, Korea. -
Flow Reagents Single Color Antibodies CD Chart
CD CHART CD N° Alternative Name CD N° Alternative Name CD N° Alternative Name Beckman Coulter Clone Beckman Coulter Clone Beckman Coulter Clone T Cells B Cells Granulocytes NK Cells Macrophages/Monocytes Platelets Erythrocytes Stem Cells Dendritic Cells Endothelial Cells Epithelial Cells T Cells B Cells Granulocytes NK Cells Macrophages/Monocytes Platelets Erythrocytes Stem Cells Dendritic Cells Endothelial Cells Epithelial Cells T Cells B Cells Granulocytes NK Cells Macrophages/Monocytes Platelets Erythrocytes Stem Cells Dendritic Cells Endothelial Cells Epithelial Cells CD1a T6, R4, HTA1 Act p n n p n n S l CD99 MIC2 gene product, E2 p p p CD223 LAG-3 (Lymphocyte activation gene 3) Act n Act p n CD1b R1 Act p n n p n n S CD99R restricted CD99 p p CD224 GGT (γ-glutamyl transferase) p p p p p p CD1c R7, M241 Act S n n p n n S l CD100 SEMA4D (semaphorin 4D) p Low p p p n n CD225 Leu13, interferon induced transmembrane protein 1 (IFITM1). p p p p p CD1d R3 Act S n n Low n n S Intest CD101 V7, P126 Act n p n p n n p CD226 DNAM-1, PTA-1 Act n Act Act Act n p n CD1e R2 n n n n S CD102 ICAM-2 (intercellular adhesion molecule-2) p p n p Folli p CD227 MUC1, mucin 1, episialin, PUM, PEM, EMA, DF3, H23 Act p CD2 T11; Tp50; sheep red blood cell (SRBC) receptor; LFA-2 p S n p n n l CD103 HML-1 (human mucosal lymphocytes antigen 1), integrin aE chain S n n n n n n n l CD228 Melanotransferrin (MT), p97 p p CD3 T3, CD3 complex p n n n n n n n n n l CD104 integrin b4 chain; TSP-1180 n n n n n n n p p CD229 Ly9, T-lymphocyte surface antigen p p n p n -
CD Markers Are Routinely Used for the Immunophenotyping of Cells
ptglab.com 1 CD MARKER ANTIBODIES www.ptglab.com Introduction The cluster of differentiation (abbreviated as CD) is a protocol used for the identification and investigation of cell surface molecules. So-called CD markers are routinely used for the immunophenotyping of cells. Despite this use, they are not limited to roles in the immune system and perform a variety of roles in cell differentiation, adhesion, migration, blood clotting, gamete fertilization, amino acid transport and apoptosis, among many others. As such, Proteintech’s mini catalog featuring its antibodies targeting CD markers is applicable to a wide range of research disciplines. PRODUCT FOCUS PECAM1 Platelet endothelial cell adhesion of blood vessels – making up a large portion molecule-1 (PECAM1), also known as cluster of its intracellular junctions. PECAM-1 is also CD Number of differentiation 31 (CD31), is a member of present on the surface of hematopoietic the immunoglobulin gene superfamily of cell cells and immune cells including platelets, CD31 adhesion molecules. It is highly expressed monocytes, neutrophils, natural killer cells, on the surface of the endothelium – the thin megakaryocytes and some types of T-cell. Catalog Number layer of endothelial cells lining the interior 11256-1-AP Type Rabbit Polyclonal Applications ELISA, FC, IF, IHC, IP, WB 16 Publications Immunohistochemical of paraffin-embedded Figure 1: Immunofluorescence staining human hepatocirrhosis using PECAM1, CD31 of PECAM1 (11256-1-AP), Alexa 488 goat antibody (11265-1-AP) at a dilution of 1:50 anti-rabbit (green), and smooth muscle KD/KO Validated (40x objective). alpha-actin (red), courtesy of Nicola Smart. PECAM1: Customer Testimonial Nicola Smart, a cardiovascular researcher “As you can see [the immunostaining] is and a group leader at the University of extremely clean and specific [and] displays Oxford, has said of the PECAM1 antibody strong intercellular junction expression, (11265-1-AP) that it “worked beautifully as expected for a cell adhesion molecule.” on every occasion I’ve tried it.” Proteintech thanks Dr. -
Regulation of Decay Accelerating Factor Primes Human Germinal Center B Cells for Phagocytosis
ORIGINAL RESEARCH published: 05 January 2021 doi: 10.3389/fimmu.2020.599647 Regulation of Decay Accelerating Factor Primes Human Germinal Center B Cells for Phagocytosis Andy Dernstedt 1, Jana Leidig 1, Anna Holm 2, Priscilla F. Kerkman 1, Jenny Mjösberg 3, Clas Ahlm 1, Johan Henriksson 4, Magnus Hultdin 5 and Mattias N. E. Forsell 1* 1 Department of Clinical Microbiology, Section of Infection and Immunology, Umeå University, Umeå, Sweden, 2 Department of Clinical Sciences, Division of Otorhinolaryngology, Umeå University, Umeå, Sweden, 3 Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden, 4 Molecular Infection Medicine Sweden, Department of Molecular Biology, Umeå University, Umeå, Sweden, 5 Department of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden Germinal centers (GC) are sites for extensive B cell proliferation and homeostasis is maintained by programmed cell death. The complement regulatory protein Decay Edited by: Accelerating Factor (DAF) blocks complement deposition on host cells and therefore Judith Fraussen, also phagocytosis of cells. Here, we show that B cells downregulate DAF upon BCR University of Hasselt, Belgium lo Reviewed by: engagement and that T cell-dependent stimuli preferentially led to activation of DAF B lo Paolo Casali, cells. Consistent with this, a majority of light and dark zone GC B cells were DAF and University of Texas Health Science susceptible to complement-dependent phagocytosis, as compared with DAFhi GC B Center at San Antonio, United States hi Shengli Xu, cells. We could also show that the DAF GC B cell subset had increased expression of the Bioprocessing Technology Institute plasma cell marker Blimp-1. -
LP Review Published.Pdf
Molecular Immunology 56 (2013) 413–422 Contents lists available at SciVerse ScienceDirect Molecular Immunology jo urnal homepage: www.elsevier.com/locate/molimm Review Toward a structure-based comprehension of the lectin pathway of complement a a b,∗ Troels R. Kjaer , Steffen Thiel , Gregers R. Andersen a Department of Biomedicine, Aarhus University, Wilhelm Meyers Allé 4, DK-8000 Aarhus, Denmark b Department of Molecular Biology and Genetics, Aarhus University, Gustav Wieds Vej 10C, DK-8000 Aarhus, Denmark a r t a b i c l e i n f o s t r a c t Article history: To initiate the lectin pathway of complement pattern recognition molecules bind to surface-linked car- Received 2 May 2013 bohydrates or acetyl groups on pathogens or damaged self-tissue. This leads to activation of the serine Accepted 14 May 2013 proteases MASP-1 and MASP-2 resulting in deposition of C4 on the activator and assembly of the C3 convertase. In addition MASP-3 and the non-catalytic MAp19 and MAp44 presumably play regulatory Keywords: functions, but the exact function of the MASP-3 protease remains to be established. Recent functional Complement system studies have significantly advanced our understanding of the molecular events occurring as activation Pattern recognition progresses from pattern recognition to convertase assembly. Furthermore, atomic structures derived MBL MASP by crystallography or solution scattering of most proteins acting in the lectin pathway and two key complexes have become available. Here we integrate the current functional and structural knowledge Protease activation C4 concerning the lectin pathway proteins and derive overall models for their glycan bound complexes. -
Hereditary Angioedema: a Broad Review for Clinicians
REVIEW ARTICLE Hereditary Angioedema A Broad Review for Clinicians Ugochukwu C. Nzeako, MD, MPH; Evangelo Frigas, MD; William J. Tremaine, MD ereditary angioedema (HAE) is an autosomal dominant disease that afflicts 1 in 10000 to 1 in 150000 persons; HAE has been reported in all races, and no sex predomi- nance has been found. It manifests as recurrent attacks of intense, massive, localized edema without concomitant pruritus, often resulting from one of several known trig- Hgers. However, attacks can occur in the absence of any identifiable initiating event. Historically, 2 types of HAE have been described. However, a variant, possibly X-linked, inherited angioedema has recently been described, and tentatively it has been named “type 3” HAE. Signs and symptoms are identical in all types of HAE. Skin and visceral organs may be involved by the typically massive local edema. The most commonly involved viscera are the respiratory and gastrointestinal sys- tems. Involvement of the upper airways can result in severe life-threatening symptoms, including the risk of asphyxiation, unless appropriate interventions are taken. Quantitative and functional analyses of C1 esterase inhibitor and complement components C4 and C1q should be performed when HAE is suspected. Acute exacerbations of the disease should be treated with intravenous purified C1 esterase inhibitor concentrate, where available. Intravenous administration of fresh frozen plasma is also useful in acute HAE; however, it occasionally exacerbates symptoms. Corti- costeroids, antihistamines, and epinephrine can be useful adjuncts but typically are not effica- cious in aborting acute attacks. Prophylactic management involves long-term use of attenuated androgens or antifibrinolytic agents.