Complement Receptors 1 and 2 HECTOR MOLINA*T, V
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PAX5 Expression in Acute Leukemias: Higher B-Lineage Specificity Than Cd79a and Selective Association with T(8;21)-Acute Myelogenous Leukemia
[CANCER RESEARCH 64, 7399–7404, October 15, 2004] PAX5 Expression in Acute Leukemias: Higher B-Lineage Specificity Than CD79a and Selective Association with t(8;21)-Acute Myelogenous Leukemia Enrico Tiacci,1 Stefano Pileri,2 Annette Orleth,1 Roberta Pacini,1 Alessia Tabarrini,1 Federica Frenguelli,1 Arcangelo Liso,3 Daniela Diverio,4 Francesco Lo-Coco,5 and Brunangelo Falini1 1Institutes of Hematology and Internal Medicine, University of Perugia, Perugia, Italy; 2Unit of Hematopathology, University of Bologne, Bologne, Italy; 3Section of Hematology, University of Foggia, Foggia, Italy; 4Department of Cellular Biotechnologies and Hematology, University La Sapienza of Rome, Rome, Italy; and 5Department of Biopathology, University Tor Vergata of Rome, Rome, Italy ABSTRACT (13, 16). PAX5 expression also occurs in the adult testis and in the mesencephalon and spinal cord during embryogenesis (17), suggesting an The transcription factor PAX5 plays a key role in the commitment of important role in the development of these tissues. hematopoietic precursors to the B-cell lineage, but its expression in acute Rearrangement of the PAX5 gene through reciprocal chromosomal leukemias has not been thoroughly investigated. Hereby, we analyzed routine biopsies from 360 acute leukemias of lymphoid (ALLs) and mye- translocations has been described in different types of B-cell malig- loid (AMLs) origin with a specific anti-PAX5 monoclonal antibody. Blasts nancies (18–23), and, more recently, PAX5 has also been shown to be from 150 B-cell ALLs showed strong PAX5 nuclear expression, paralleling targeted by aberrant hypermutation in Ͼ50% of diffuse large B-cell that of CD79a in the cytoplasm. Conversely, PAX5 was not detected in 50 lymphomas (24). -
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. -
Bispecific CAR-T Cells Targeting Both CD19 and CD22 for Therapy Of
Dai et al. Journal of Hematology & Oncology (2020) 13:30 https://doi.org/10.1186/s13045-020-00856-8 RAPID COMMUNICATION Open Access Bispecific CAR-T cells targeting both CD19 and CD22 for therapy of adults with relapsed or refractory B cell acute lymphoblastic leukemia Hanren Dai1,2,3†, Zhiqiang Wu1†, Hejin Jia2†, Chuan Tong1, Yelei Guo1, Dongdong Ti1, Xiao Han1, Yang Liu4, Wenying Zhang2, Chunmeng Wang2, Yajing Zhang2, Meixia Chen2, Qingming Yang2, Yao Wang1* and Weidong Han1,2* Abstract Background: Despite the impressive complete remission (CR) induced by CD19 CAR-T cell therapy in B-ALL, the high rate of complete responses is sometimes limited by the emergence of CD19-negative leukemia. Bispecific CAR-modified T cells targeting both CD19 and CD22 may overcome the limitation of CD19-negative relapse. Methods: We here report the design of a bispecific CAR simultaneous targeting of CD19 and CD22. We performed a phase 1 trial of bispecific CAR T cell therapy in patients with relapsed/refractory precursor B-ALL at a dose that ranged from 1.7 × 106 to 3 × 106 CAR T cells per kilogram of body weight. Results: We demonstrate bispecific CD19/CD22 CAR T cells could trigger robust cytolytic activity against target cells. MRD-negative CR was achieved in 6 out of 6 enrolled patients. Autologous CD19/CD22 CAR T cells proliferated in vivo and were detected in the blood, bone marrow, and cerebrospinal fluid. No neurotoxicity occurred in any of the 6 patients treated. Of note, one patient had a relapse with blast cells that no longer expressed CD19 and exhibited diminished CD22 site density approximately 5 months after treatment. -
Role of IL-4 Receptor &Alpha
Role of IL-4 receptor a–positive CD41 T cells in chronic airway hyperresponsiveness Frank Kirstein, PhD, Natalie E. Nieuwenhuizen, PhD,* Jaisubash Jayakumar, PhD, William G. C. Horsnell, PhD, and Frank Brombacher, PhD Cape Town, South Africa, and Berlin, Germany Background: TH2 cells and their cytokines are associated with IL-17–producing T cells and, consequently, increased airway allergic asthma in human subjects and with mouse models of neutrophilia. allergic airway disease. IL-4 signaling through the IL-4 receptor Conclusion: IL-4–responsive T helper cells are dispensable for 1 a (IL-4Ra) chain on CD4 T cells leads to TH2 cell acute OVA-induced airway disease but crucial in maintaining differentiation in vitro, implying that IL-4Ra–responsive CD41 chronic asthmatic pathology. (J Allergy Clin Immunol T cells are critical for the induction of allergic asthma. However, 2016;137:1852-62.) mechanisms regulating acute and chronic allergen-specific T 2 H Key words: responses in vivo remain incompletely understood. TH2 cell, acute allergic airway disease, chronic asthma, Objective: This study defines the requirements for IL-4Ra– cytokine receptors, IL-4, IL-13, gene-deficient mice responsive CD41 T cells and the IL-4Ra ligands IL-4 and IL-13 in the development of allergen-specific TH2 responses during the Allergic asthma is a chronic inflammatory disease of the airways onset and chronic phase of experimental allergic airway disease. characterized by an inappropriate immune response to harmless Methods: Development of acute and chronic ovalbumin environmental antigens. T 2 cells regulate adaptive immune 1 H (OVA)–induced allergic asthma was assessed weekly in CD4 T responses to allergens, and their presence correlates with disease 2 cell–specific IL-4Ra–deficient BALB/c mice (LckcreIL-4Ra /lox) symptoms in human subjects and mice.1 IL-4 plays a crucial role and respective control mice in the presence or absence of IL-4 in the in vitro and in vivo differentiation of TH2 cells, suggesting or IL-13. -
List of Genes Used in Cell Type Enrichment Analysis
List of genes used in cell type enrichment analysis Metagene Cell type Immunity ADAM28 Activated B cell Adaptive CD180 Activated B cell Adaptive CD79B Activated B cell Adaptive BLK Activated B cell Adaptive CD19 Activated B cell Adaptive MS4A1 Activated B cell Adaptive TNFRSF17 Activated B cell Adaptive IGHM Activated B cell Adaptive GNG7 Activated B cell Adaptive MICAL3 Activated B cell Adaptive SPIB Activated B cell Adaptive HLA-DOB Activated B cell Adaptive IGKC Activated B cell Adaptive PNOC Activated B cell Adaptive FCRL2 Activated B cell Adaptive BACH2 Activated B cell Adaptive CR2 Activated B cell Adaptive TCL1A Activated B cell Adaptive AKNA Activated B cell Adaptive ARHGAP25 Activated B cell Adaptive CCL21 Activated B cell Adaptive CD27 Activated B cell Adaptive CD38 Activated B cell Adaptive CLEC17A Activated B cell Adaptive CLEC9A Activated B cell Adaptive CLECL1 Activated B cell Adaptive AIM2 Activated CD4 T cell Adaptive BIRC3 Activated CD4 T cell Adaptive BRIP1 Activated CD4 T cell Adaptive CCL20 Activated CD4 T cell Adaptive CCL4 Activated CD4 T cell Adaptive CCL5 Activated CD4 T cell Adaptive CCNB1 Activated CD4 T cell Adaptive CCR7 Activated CD4 T cell Adaptive DUSP2 Activated CD4 T cell Adaptive ESCO2 Activated CD4 T cell Adaptive ETS1 Activated CD4 T cell Adaptive EXO1 Activated CD4 T cell Adaptive EXOC6 Activated CD4 T cell Adaptive IARS Activated CD4 T cell Adaptive ITK Activated CD4 T cell Adaptive KIF11 Activated CD4 T cell Adaptive KNTC1 Activated CD4 T cell Adaptive NUF2 Activated CD4 T cell Adaptive PRC1 Activated -
T Cells the Usual Subsets
T cells: the usual subsets Chen Dong and Gustavo J. Martinez T cells have important roles in immune responses and function by directly secreting soluble mediators or important for adaptation of immune responses in different microenvironments and might be particularly through cell contact-dependent mechanisms. Many T cell subsets have been characterized. Although relevant for host defence against pathogens that colonize different tissues. Distinct T cell subsets, or effector T cells were originally considered to be terminally differentiated, a growing body of evidence has differentiation states, can be identified based on the cell surface markers expressed and/or the effector challenged this view and suggested that the phenotype of effector T cells is not completely fixed but is molecules produced by a particular T cell population. This Poster summarizes our current understanding of more flexible or plastic. T cells can have ‘mixed’ phenotypes (that is, have characteristics usually the surface markers, transcriptional regulators, effector molecules and functions of the different T cell associated with more than one T cell subset) and can interconvert from one subset phenotype to another, subsets that participate in immune responses. Further knowledge of how these T cell subsets are regulated IMMUNOLOGY although instructive signalling can lead to long-term fixation of cytokine memory. T cell plasticity can be and cooperate with each other will provide us with better tools to treat immune-related diseases. Cytotoxic T cell Exhausted T cell -
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. -
Genetic Susceptibility to Chronic Wasting Disease in Free-Ranging White-Tailed Deer: Complement Component C1q and Prnp Polymorphisms Julie A
Natural Resource Ecology and Management Natural Resource Ecology and Management Publications 12-2009 Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms Julie A. Blanchong Iowa State University, [email protected] Dennis M. Heisey United States Geological Survey Kim T. Scribner Michigan State University Scot V. Libants Michigan State University Chad Johnson UFonilvloerwsit ythi of sW aiscondn asiddn - itMionadisoaln works at: http://lib.dr.iastate.edu/nrem_pubs Part of the Animal Diseases Commons, Genetics Commons, Natural Resources Management See next page for additional authors and Policy Commons, Veterinary Infectious Diseases Commons, and the Zoology Commons The ompc lete bibliographic information for this item can be found at http://lib.dr.iastate.edu/ nrem_pubs/84. For information on how to cite this item, please visit http://lib.dr.iastate.edu/ howtocite.html. This Article is brought to you for free and open access by the Natural Resource Ecology and Management at Iowa State University Digital Repository. It has been accepted for inclusion in Natural Resource Ecology and Management Publications by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. Genetic susceptibility to chronic wasting disease in free-ranging white- tailed deer: Complement component C1q and Prnp polymorphisms Abstract The eg netic basis of susceptibility to chronic wasting disease (CWD) in free-ranging cervids is of great interest. Association studies of disease susceptibility in free-ranging populations, however, face considerable challenges including: the need for large sample sizes when disease is rare, animals of unknown pedigree create a risk of spurious results due to population admixture, and the inability to control disease exposure or dose. -
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, -
T Lymphocytes + and CD8 +CD4 TCR/CD3 Complex in Immortalized Mature -Deficient Γ Signaling Through A
Signaling Through a CD3γ-Deficient TCR/CD3 Complex in Immortalized Mature CD4+ and CD8+ T Lymphocytes This information is current as Alberto Pacheco-Castro, David Alvarez-Zapata, Pilar of September 25, 2021. Serrano-Torres and José R. Regueiro J Immunol 1998; 161:3152-3160; ; http://www.jimmunol.org/content/161/6/3152 Downloaded from References This article cites 47 articles, 19 of which you can access for free at: http://www.jimmunol.org/content/161/6/3152.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 25, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 1998 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Signaling Through a CD3g-Deficient TCR/CD3 Complex in Immortalized Mature CD41 and CD81 T Lymphocytes1 Alberto Pacheco-Castro,2 David Alvarez-Zapata,2 Pilar Serrano-Torres, and Jose´R. Regueiro3 The biologic role of each CD3 chain and their relative contribution to the signals transduced through the TCR/CD3 complex and to downstream activation events are still controversial: they may be specialized or redundant. -
18F-Farag PET for CD8 Profiling of Tumors and Assessment of Immunomodulation by Chemotherapy
Journal of Nuclear Medicine, published on November 6, 2020 as doi:10.2967/jnumed.120.249078 18F-FAraG PET for CD8 Profiling of Tumors and Assessment of Immunomodulation by Chemotherapy Jelena Levi1*, Samuel Goth1, Lyna Huynh1, Tina Lam1, Tony L Huynh2, Brailee Schulte2, Juliet A Packiasamy1 1CellSight Technologies Incorporated, San Francisco, California; 2Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, California; *Corresponding Author Jelena Levi, PhD 185 Berry street, San Francisco, 94107, CA Email: [email protected] Running Title: [18F]F-AraG for CD8 profiling of tumors Financial statement: This work was supported by National Institutes of Health Grants NCI SBIR HHSN261201800024C (JL). Conflict of Interest Statement: JL, SG, LH, TL and JP are or were employed by CellSight Technologies. CellSight Technologies Incorporated is commercializing [18F]F-AraG as a PET tracer for evaluation of immune response in immunotherapy. No other potential conflicts of interest relevant to this article exist. ABSTRACT Majority of the clinical trials exploring various combinations of chemo- and immunotherapy rely on serial biopsy to provide information on immune response. The aim of this study was to assess the value of 18F-FAraG as a non-invasive tool that could profile tumors based on the key players in adaptive antitumor response, CD8+ cells, and evaluate immunomodulatory effects of chemotherapy. Methods. To evaluate the ability of 18F-FAraG to report on the presence of CD8+ cells within the TME, we imaged a panel of syngeneic tumor models (MC38, CT26, LLC, A9F1, 4T1 and B16F10), and correlated the signal intensity with the number of lymphocytes found in the tumors. -
Neutrophil Chemoattractant Receptors in Health and Disease: Double-Edged Swords
Cellular & Molecular Immunology www.nature.com/cmi REVIEW ARTICLE Neutrophil chemoattractant receptors in health and disease: double-edged swords Mieke Metzemaekers1, Mieke Gouwy1 and Paul Proost 1 Neutrophils are frontline cells of the innate immune system. These effector leukocytes are equipped with intriguing antimicrobial machinery and consequently display high cytotoxic potential. Accurate neutrophil recruitment is essential to combat microbes and to restore homeostasis, for inflammation modulation and resolution, wound healing and tissue repair. After fulfilling the appropriate effector functions, however, dampening neutrophil activation and infiltration is crucial to prevent damage to the host. In humans, chemoattractant molecules can be categorized into four biochemical families, i.e., chemotactic lipids, formyl peptides, complement anaphylatoxins and chemokines. They are critically involved in the tight regulation of neutrophil bone marrow storage and egress and in spatial and temporal neutrophil trafficking between organs. Chemoattractants function by activating dedicated heptahelical G protein-coupled receptors (GPCRs). In addition, emerging evidence suggests an important role for atypical chemoattractant receptors (ACKRs) that do not couple to G proteins in fine-tuning neutrophil migratory and functional responses. The expression levels of chemoattractant receptors are dependent on the level of neutrophil maturation and state of activation, with a pivotal modulatory role for the (inflammatory) environment. Here, we provide an overview