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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. -
A Fratricide-Resistant Allogeneic CAR T
Investigation of ALLO-316: A Fratricide- Resistant Allogeneic CAR T Targeting CD70 As a Potential Therapy for the Treatment of AML Surabhi Srinivasan, Nguyen Tan, Hsin-Yuan Cheng, Yi Zhang, Silvia Tacheva-Grigorova, Tom Van Blarcom, Cesar Sommer, Duy Nguyen , Barbra Sasu, and Siler Panowski 1 Disclosures • Full-time employee of Allogene Therapeutics • Equity interest in Allogene Therapeutics ALLO-316 (CD70) utilizes TALEN® gene-editing technology pioneered and owned by Cellectis. Allogene has an exclusive license to the Cellectis technology for allogeneic products directed at this target and holds all global development and commercial rights for this investigational candidate. 22 CONFIDENTIAL Disclaimers This presentation is not intended for product promotion. All information is related to investigational therapies not available for commercial use. The safety and efficacy of the therapies have not been established for FDA approval. Forward-Looking Statements To the extent statements contained in this Presentation are not descriptions of historical facts regarding Allogene Therapeutics, Inc. (“Allogene,” “we,” “us,” or “our”), they are forward-looking statements reflecting management’s current beliefs and expectations. Forward-looking statements are subject to known and unknown risks, uncertainties, and other factors that may cause our or our industry’s actual results, levels or activity, performance, or achievements to be materially different from those anticipated by such statements. You can identify forward-looking statements by words such as “anticipate,” “believe,” “could,” “estimate,” “expect,” “intend,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “will,” “would” or the negative of those terms, and similar expressions that convey uncertainty of future events or outcomes. Forward-looking statements contained in this Presentation include, but are not limited to, statements regarding: the ability to progress the clinical development of allogeneic CAR T (AlloCAR T™) therapies and the potential benefits of AlloCAR T™ therapy, including ALLO-316. -
Dendritic Cell Expression of CD70 in Vivo Potent Cellular Immunity By
Combined TLR/CD40 Stimulation Mediates Potent Cellular Immunity by Regulating Dendritic Cell Expression of CD70 In Vivo This information is current as Phillip J. Sanchez, Jennifer A. McWilliams, Catherine of September 25, 2021. Haluszczak, Hideo Yagita and Ross M. Kedl J Immunol 2007; 178:1564-1572; ; doi: 10.4049/jimmunol.178.3.1564 http://www.jimmunol.org/content/178/3/1564 Downloaded from References This article cites 57 articles, 25 of which you can access for free at: http://www.jimmunol.org/content/178/3/1564.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 25, 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 © 2007 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Combined TLR/CD40 Stimulation Mediates Potent Cellular Immunity by Regulating Dendritic Cell Expression of CD70 In Vivo1 Phillip J. Sanchez,* Jennifer A. McWilliams,* Catherine Haluszczak,* Hideo Yagita,† and Ross M. Kedl2* We previously showed that immunization with a combination of TLR and CD40 agonists (combined TLR/CD40 agonist immu- nization) resulted in an expansion of Ag-specific CD8 T cells exponentially greater than the expansion observed to immunization with either agonist alone. -
Gene Symbol Category ACAN ECM ADAM10 ECM Remodeling-Related ADAM11 ECM Remodeling-Related ADAM12 ECM Remodeling-Related ADAM15 E
Supplementary Material (ESI) for Integrative Biology This journal is (c) The Royal Society of Chemistry 2010 Gene symbol Category ACAN ECM ADAM10 ECM remodeling-related ADAM11 ECM remodeling-related ADAM12 ECM remodeling-related ADAM15 ECM remodeling-related ADAM17 ECM remodeling-related ADAM18 ECM remodeling-related ADAM19 ECM remodeling-related ADAM2 ECM remodeling-related ADAM20 ECM remodeling-related ADAM21 ECM remodeling-related ADAM22 ECM remodeling-related ADAM23 ECM remodeling-related ADAM28 ECM remodeling-related ADAM29 ECM remodeling-related ADAM3 ECM remodeling-related ADAM30 ECM remodeling-related ADAM5 ECM remodeling-related ADAM7 ECM remodeling-related ADAM8 ECM remodeling-related ADAM9 ECM remodeling-related ADAMTS1 ECM remodeling-related ADAMTS10 ECM remodeling-related ADAMTS12 ECM remodeling-related ADAMTS13 ECM remodeling-related ADAMTS14 ECM remodeling-related ADAMTS15 ECM remodeling-related ADAMTS16 ECM remodeling-related ADAMTS17 ECM remodeling-related ADAMTS18 ECM remodeling-related ADAMTS19 ECM remodeling-related ADAMTS2 ECM remodeling-related ADAMTS20 ECM remodeling-related ADAMTS3 ECM remodeling-related ADAMTS4 ECM remodeling-related ADAMTS5 ECM remodeling-related ADAMTS6 ECM remodeling-related ADAMTS7 ECM remodeling-related ADAMTS8 ECM remodeling-related ADAMTS9 ECM remodeling-related ADAMTSL1 ECM remodeling-related ADAMTSL2 ECM remodeling-related ADAMTSL3 ECM remodeling-related ADAMTSL4 ECM remodeling-related ADAMTSL5 ECM remodeling-related AGRIN ECM ALCAM Cell-cell adhesion ANGPT1 Soluble factors and receptors -
Belongs to the TNF Family a New Class of Reverse Signaling
A New Class of Reverse Signaling Costimulators Belongs to the TNF Family Mingyi Sun and Pamela J. Fink This information is current as J Immunol 2007; 179:4307-4312; ; of September 27, 2021. doi: 10.4049/jimmunol.179.7.4307 http://www.jimmunol.org/content/179/7/4307 References This article cites 85 articles, 38 of which you can access for free at: Downloaded from http://www.jimmunol.org/content/179/7/4307.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision http://www.jimmunol.org/ • 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: by guest on September 27, 2021 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 © 2007 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. THE JOURNAL OF IMMUNOLOGY BRIEF REVIEWS A New Class of Reverse Signaling Costimulators Belongs to the TNF Family Mingyi Sun and Pamela J. Fink1 Recent evidence shows that many molecules of the TNF still remains unclear (7). The N-terminal cytoplasmic domains family serve as counter-receptors, inducing costimulation of most TNF family members are conserved across species but through reverse signals in addition to delivering signals not between family members, suggesting that the intracellular through their respective TNF receptors. -
CD95 Ligand - Death Factor and Costimulatory Molecule?
Cell Death and Differentiation (2003) 10, 1215–1225 & 2003 Nature Publishing Group All rights reserved 1350-9047/03 $25.00 www.nature.com/cdd Review CD95 ligand - death factor and costimulatory molecule? O Janssen*,1, J Qian1, A Linkermann1 and D Kabelitz1 Tissue and Cellular Expression of CD95L 1 Institute for Immunology, Medical Center Schleswig-Holstein, Campus Kiel, Michaelisstrasse 5, D-24105 Kiel, Germany The CD95 ligand (CD95L, Apo-1L, FasL, CD178) is a 281- * Corresponding author: O Janssen. Tel: þ 49-431-5973377; Fax: þ 49-431- amino-acid-containing type II transmembrane protein of the 5973335; E-mail: [email protected] TNF family of death factors (Figure 1).1 Its death-inducing function is best documented in the context of activation- Received 24.4.03; revised 12.6.03; accepted 20.6.03; published online 1 August 2003 induced cell death (AICD) in T cells.2 CD95L is expressed as a Edited by T Ferguson death factor in cytotoxic T lymphocytes (CTL) to kill virally infected or transformed target cells and in natural killer (NK) cells, where it is upregulated by CD16 engagement and 3 Abstract cytokines including IL-2 and IL-12. Similarly, high levels of intracellular CD95L have been detected in monocytic cells The CD95 ligand is involved as a death factor in the with an inducible release upon activation.4 Under physiologi- regulation of activation-induced cell death, establishment cal conditions, CD95L is implicated in the control of erythroid of immune privilege and tumor cell survival. In addition, differentiation,5 angiogenesis in the eye6 and skin home- 7 CD95L may serve as a costimulatory molecule for T-cell ostasis. -
Immunosenescence: a Key Player in Cancer Development Jingyao Lian1,2†, Ying Yue1,2,3†, Weina Yu1,2† and Yi Zhang1,2*
Lian et al. J Hematol Oncol (2020) 13:151 https://doi.org/10.1186/s13045-020-00986-z REVIEW Open Access Immunosenescence: a key player in cancer development Jingyao Lian1,2†, Ying Yue1,2,3†, Weina Yu1,2† and Yi Zhang1,2* Abstract Immunosenescence is a process of immune dysfunction that occurs with age and includes remodeling of lymphoid organs, leading to changes in the immune function of the elderly, which is closely related to the development of infections, autoimmune diseases, and malignant tumors. T cell–output decline is an important feature of immunose- nescence as well as the production of senescence-associated secretory phenotype, increased glycolysis, and reactive oxygen species. Senescent T cells exhibit abnormal phenotypes, including downregulation of CD27, CD28, and upreg- ulation of CD57, killer cell lectin-like receptor subfamily G, Tim-3, Tight, and cytotoxic T-lymphocyte-associated protein 4, which are tightly related to malignant tumors. The role of immunosenescence in tumors is sophisticated: the many factors involved include cAMP, glucose competition, and oncogenic stress in the tumor microenvironment, which can induce the senescence of T cells, macrophages, natural killer cells, and dendritic cells. Accordingly, these senescent immune cells could also afect tumor progression. In addition, the efect of immunosenescence on the response to immune checkpoint blocking antibody therapy so far is ambiguous due to the low participation of elderly cancer patients in clinical trials. Furthermore, many other senescence-related interventions could be possible with genetic and pharmacological methods, including mTOR inhibition, interleukin-7 recombination, and NAD + activation. Overall, this review aims to highlight the characteristics of immunosenescence and its impact on malignant tumors and immunotherapy, especially the future directions of tumor treatment through senescence-focused strategies. -
Co-Expression of CD40L with CD70 Or OX40L Increases B-Cell Viability and Antitumor Efficacy
www.impactjournals.com/oncotarget/ Oncotarget, Vol. 7, No. 29 Research Paper Co-expression of CD40L with CD70 or OX40L increases B-cell viability and antitumor efficacy Chang-Ae Shin1, Hyun-Woo Cho1, A-Ri Shin2,3, Hyun-Jung Sohn2, Hyun-Il Cho2,3, Tai-Gyu Kim1,2,3 1Department of Microbiology and Immunology, College of Medicine, The Catholic University of Korea, Seoul 137-701, South Korea 2Catholic Hematopoietic Stem Cell Bank, College of Medicine, The Catholic University of Korea, Seoul 137-701, South Korea 3Catholic Cancer Research Institute, College of Medicine, The Catholic University of Korea, Seoul 137-701, South Korea Correspondence to: Hyun-Il Cho, email: [email protected] Tai-Gyu Kim, email: [email protected] Keywords: cancer vaccine, B-cells, costimulatory ligand, anti-apoptosis, tumor immunity Received: February 24, 2016 Accepted: May 29, 2016 Published: June 15, 2016 ABSTRACT Activated B-cells are a promising alternative source of antigen-presenting cells. They can generally be obtained in sufficient numbers for clinical use, but in most instances produce weak immune responses and therapeutic effects that are suboptimal for use in therapeutic cancer vaccines. To improve the immunogenic potency and therapeutic efficacy of B-cell-based vaccines, ex vivo-activated B-cells were transduced with recombinant lentiviruses in order to express additional costimulatory ligands—CD40L, CD70, OX40L, or 4-1BBL—either individually or in pairs (CD70/CD40L, OX40L/CD40L, or 4-1BBL/CD40L). We observed that the expression of CD40L molecules on B-cells was crucial for T-cell priming and activation. Administration of B-cells co-expressing CD40L with the other costimulatory ligands provided substantial antigen-specific CD8 T-cell responses capable of provoking in vivo proliferation and potent cytolytic activities. -
Snapshot: Cytokines III Cristina M
SnapShot: Cytokines III Cristina M. Tato and Daniel J. Cua Schering-Plough Biopharma (Formerly DNAX Research), Palo Alto, CA 94304, USA Cytokine Receptor Source Targets Major Function Disease Association TNFα Murine: Macrophages, Neutrophils, Inflammatory; ↓ = disregulated fever; increased TNFR,p55; TNFR,p75 monocytes, T cells, macrophages, promotes activation susceptibility to bacterial infection; others monocytes, and production of enhanced resistance to LPS-induced septic Human: endothelial cells acute-phase proteins shock TNFR,p60; TNFR,p80 ↑ = exacerbation of arthritis and colitis LTα Murine: T cells, B cells Many cell types Promotes activation ↓ = defective response to bacterial TNFR,p55; TNFR,p75 and cytotoxicity; pathogens; absence of peripheral lymph development of lymph nodes and Peyer’s patches Human: nodes and Peyer’s TNFR,p60; TNFR,p80 patches LTβ LTβR T cells, B cells Myeloid cells, other Peripheral lymph ↓ = increased susceptibility to bacterial cell types node development; infection; absence of lymph nodes and proinflammatory Peyer’s patches ↑ = ectopic lymph node formation LIGHTa LTβR, DcR3, HVEM Activated T cells, B cells, NK cells, Costimulatory; ↓ = defective CD8 T cell costimulation monocytes, DCs DCs, other tissue promotes CTL activity TWEAK Fn14 Monocytes, Tissue progenitors, Proinflammatory; macrophages, epithelial, promotes cell growth endothelial endothelial for tissue repair and remodeling APRIL TACI, BAFF-R, BCMA Macrophages, DCs B cell subsets Promotes T cell- ↓ = impaired class switching to IgA independent -
Molecular Biology of Hodgkin Lymphoma
Leukemia (2021) 35:968–981 https://doi.org/10.1038/s41375-021-01204-6 REVIEW ARTICLE Lymphoma Molecular biology of Hodgkin lymphoma 1 1 Marc A. Weniger ● Ralf Küppers Received: 17 November 2020 / Revised: 1 February 2021 / Accepted: 18 February 2021 / Published online: 8 March 2021 © The Author(s) 2021. This article is published with open access Abstract Classical Hodgkin lymphoma (cHL) is unique among lymphoid malignancies in several key biological features. (i) The Hodgkin and Reed-Sternberg (HRS) tumor cells are rare among an extensive and complex microenvironment. (ii) They derive from B cells, but have largely lost the B-cell typical gene expression program. (iii) Their specific origin appears to be pre-apoptotic germinal center (GC) B cells. (iv) They consistently develop bi- or multinucleated Reed-Sternberg cells from mononuclear Hodgkin cells. (v) They show constitutive activation of numerous signaling pathways. Recent studies have begun to uncover the basis of these specific features of cHL: HRS cells actively orchestrate their complex microenvironment and attract many distinct subsets of immune cells into the affected tissues, to support their survival and proliferation, and to create an immunosuppressive environment. Reed-Sternberg cells are generated by incomplete cytokinesis and refusion of Hodgkin cells. Epstein-Barr virus (EBV) plays a major role in the rescue of crippled GC B cells 1234567890();,: 1234567890();,: from apoptosis and hence is a main player in early steps of lymphomagenesis of EBV+ cHL cases. The analysis of the landscape of genetic lesions in HRS cells so far did not reveal any highly recurrent HRS cell-specific lesions, but major roles of genetic lesions in members of the NF-κB and JAK/STAT pathways and of factors of immune evasion. -
Identification of Novel CD4+ T Cell Subsets in the Target Tissue Of
Identification of Novel CD4+ T Cell Subsets in the Target Tissue of Sjögren's Syndrome and Their Differential Regulation by the Lymphotoxin/LIGHT Signaling Axis This information is current as of October 2, 2021. Scott Haskett, Jian Ding, Wei Zhang, Alice Thai, Patrick Cullen, Shanqin Xu, Britta Petersen, Galina Kuznetsov, Luke Jandreski, Stefan Hamann, Taylor L. Reynolds, Norm Allaire, Timothy S. Zheng and Michael Mingueneau J Immunol 2016; 197:3806-3819; Prepublished online 7 Downloaded from October 2016; doi: 10.4049/jimmunol.1600407 http://www.jimmunol.org/content/197/10/3806 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2016/10/06/jimmunol.160040 Material 7.DCSupplemental References This article cites 46 articles, 8 of which you can access for free at: http://www.jimmunol.org/content/197/10/3806.full#ref-list-1 Why The JI? Submit online. by guest on October 2, 2021 • 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 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. -
CD70 Knockout: a Novel Approach to Augment CAR-T Cell Function
#1537 CD70 knockout: A novel approach to augment CAR-T cell function Mary-Lee Dequeant, Jason Sagert, Demetri Kalaitzidis, Hui Yu, Ashley Porras, Brigid McEwan, Zinkal Padalia, Paul Tetteh, Thao Nguyen, Andrew Dunn, Sarah Spencer, Nicolette Lee, Henia Dar, Daniel Henderson, Sushant Karnik, Pooja Keerthipati, Jonathan A. Terrett CRISPR Therapeutics, 610 Main Street, Cambridge, MA, USA 02139 Abstract KO of certain checkpoint genes is detrimental to CAR-T function CD70 and its ligand, CD27, have been described as both activating and suppressing for different cell types including B and T cells. There has been speculation that the CD70/CD27 axis can act in a checkpoint or co-stimulatory manner in certain Figure 8: CD70 KO confers superior cytotoxic activity than PD1 KO against an RCC Figure 10: KO of multiple checkpoint genes impairs CAR-T cell function immuno-oncology settings. Knockout (KO) of CD70 function scored highly in a CRISPR/Cas9 screen of candidate genes for enhanced T cell activity. Deletion of other checkpoint candidates such as PD1, TIM3, LAG3 and TIGIT scored much lower than CD70, both alone and in combination with each other. T cells with CD70 KO showed resistance to exhaustion upon repeated stimulation in culture. CAR-T cells with CD70 KO similarly showed exhaustion resistance, as well as a reduction in tumor cell line overexpressing PD-L1 A Input Bone Marrow (Day 100) 10000 apoptosis, increased proliferation, and improved target cell lysis upon sequential rechallenges. CTX130 is an investigational allogeneic CAR-T therapy currently being studied in patients with CD70-expressing tumors, including clear cell renal cell 100 2500 No RNP or AAV carcinoma and B and T cell malignancies.