Tools for Cell Therapy and Immunoregulation
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Human Angiogenin Fused to Human CD30 Ligand (Ang-CD30L) Exhibits Specific Cytotoxicity Against CD30-Positive Lymphoma1
[CANCER RESEARCH 61, 8737–8742, December 15, 2001] Human Angiogenin Fused to Human CD30 Ligand (Ang-CD30L) Exhibits Specific Cytotoxicity against CD30-positive Lymphoma1 Michael Huhn, Stephanie Sasse, Mehmet K. Tur, Ba¨rbel Matthey, Timo Schinko¨the, Susanna M. Rybak, Stefan Barth,2 and Andreas Engert Fraunhofer IME, Department of Pharmaceutical Product Development, 52074 Aachen, Germany [M. K. T., M. H., S. B.]; Laboratory of Immunotherapy, Department I of Internal Medicine, University Hospital Cologne, 50931 Cologne, Germany [S. S., B. M., T. S., A. E.]; Developmental Therapeutics Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702 [S. M. R.] ABSTRACT first and then to administer ITs to kill residual H-RS cells. One of the most promising target antigens for immunotherapy of malignant lym- A number of different immunotoxins composed of cell-specific target- phoma such as Hodgkin’s lymphoma or anaplastic large cell lym- ing structures coupled to plant or bacterial toxins have increasingly been phoma is the CD30 receptor. This antigen was originally discovered evaluated for immunotherapy. Because these foreign proteins are highly immunogenic in humans, we have developed a new CD30 ligand-based on cultured H-RS cells using the moab Ki-1 (1). The gene encoding fusion toxin (Ang-CD30L) using the human RNase angiogenin. The com- the CD30 receptor molecule (2) is located on chromosome 1p36. The pletely human fusion gene was inserted into a pET-based expression naturally occurring CD30 ligand has also been identified and cloned plasmid. Transformed Escherichia coli BL21(DE3) were grown under (3). -
4-1BB Signaling Beyond T Cells
Cellular & Molecular Immunology (2011) 8, 281–284 ß 2011 CSI and USTC. All rights reserved 1672-7681/11 $32.00 www.nature.com/cmi MINI REVIEW 4-1BB signaling beyond T cells Dass S Vinay1 and Byoung S Kwon1,2 Originally discovered as a T cell-activating molecule, 4-1BB (CD137) is now also recognized as an activator of non-T cells, thus imparting a new dimension to its potential in vivo effects. 4-1BB expression is seen on a variety of non-T cells including activated dendritic cells (DCs), monocytes, neutrophils, B cells and natural killer (NK) cells, and promotes their individual effector functions. The T cell- and non-T cell-activating ability of 4-1BB may be the basis of its powerful anti-cancer, anti-autoimmune and anti-viral effects. Here we discuss the consequence and importance of 4-1BB signaling in non-T cells. We consider its effects on immune regulation, and the distinct and/or overlapping pathways involved in these responses, as well as possible therapeutic applications. Cellular & Molecular Immunology (2011) 8, 281–284; doi:10.1038/cmi.2010.82; published online 10 January 2011 Keywords: APC; cytokines; natural killer cells; T cells; 4-1BB INTRODUCTION focus on the functions of 4-1BB in non-T cells including DCs, mono- 4-1BB (CD137; TNFRSF9), discovered originally on T cells,1 is a 50- cytes, neutrophils, B cells and NK cells, and discuss how its expression to 55-kDa protein concerned with progressive immunity.2,3 4-1BB might be manipulated to treat various immune diseases. expression is in most cases activation induced. -
ENSG Gene Encodes Effector TCR Pathway Costimulation Inhibitory/Exhaustion Synapse/Adhesion Chemokines/Receptors
ENSG Gene Encodes Effector TCR pathway Costimulation Inhibitory/exhaustion Synapse/adhesion Chemokines/receptors ENSG00000111537 IFNG IFNg x ENSG00000109471 IL2 IL-2 x ENSG00000232810 TNF TNFa x ENSG00000271503 CCL5 CCL5 x x ENSG00000139187 KLRG1 Klrg1 x ENSG00000117560 FASLG Fas ligand x ENSG00000121858 TNFSF10 TRAIL x ENSG00000134545 KLRC1 Klrc1 / NKG2A x ENSG00000213809 KLRK1 Klrk1 / NKG2D x ENSG00000188389 PDCD1 PD-1 x x ENSG00000117281 CD160 CD160 x x ENSG00000134460 IL2RA IL-2 receptor x subunit alpha ENSG00000110324 IL10RA IL-10 receptor x subunit alpha ENSG00000115604 IL18R1 IL-18 receptor 1 x ENSG00000115607 IL18RAP IL-18 receptor x accessory protein ENSG00000081985 IL12RB2 IL-12 receptor x beta 2 ENSG00000186810 CXCR3 CXCR3 x x ENSG00000005844 ITGAL CD11a x ENSG00000160255 ITGB2 CD18; Integrin x x beta-2 ENSG00000156886 ITGAD CD11d x ENSG00000140678 ITGAX; CD11c x x Integrin alpha-X ENSG00000115232 ITGA4 CD49d; Integrin x x alpha-4 ENSG00000169896 ITGAM CD11b; Integrin x x alpha-M ENSG00000138378 STAT4 Stat4 x ENSG00000115415 STAT1 Stat1 x ENSG00000170581 STAT2 Stat2 x ENSG00000126561 STAT5a Stat5a x ENSG00000162434 JAK1 Jak1 x ENSG00000100453 GZMB Granzyme B x ENSG00000145649 GZMA Granzyme A x ENSG00000180644 PRF1 Perforin 1 x ENSG00000115523 GNLY Granulysin x ENSG00000100450 GZMH Granzyme H x ENSG00000113088 GZMK Granzyme K x ENSG00000057657 PRDM1 Blimp-1 x ENSG00000073861 TBX21 T-bet x ENSG00000115738 ID2 ID2 x ENSG00000176083 ZNF683 Hobit x ENSG00000137265 IRF4 Interferon x regulatory factor 4 ENSG00000140968 IRF8 Interferon -
Cd160 Mouse Shrna Plasmid (Locus ID 54215) – TR514223 | Origene
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for TR514223 Cd160 Mouse shRNA Plasmid (Locus ID 54215) Product data: Product Type: shRNA Plasmids Product Name: Cd160 Mouse shRNA Plasmid (Locus ID 54215) Locus ID: 54215 Synonyms: AU045688; By55 Vector: pRS (TR20003) Format: Retroviral plasmids Components: Cd160 - Mouse, 4 unique 29mer shRNA constructs in retroviral untagged vector(Gene ID = 54215). 5µg purified plasmid DNA per construct Non-effective 29-mer scrambled shRNA cassette in pRS Vector, TR30012, included for free. RefSeq: BC021596, NM_001163496, NM_001163497, NM_018767 Summary: CD160 antigen: Receptor on immune cells capable to deliver stimulatory or inhibitory signals that regulate cell activation and differentiation. Exists as a GPI-anchored and as a transmembrane form, each likely initiating distinct signaling pathways via phosphoinositol 3- kinase in activated NK cells and via LCK and CD247/CD3 zeta chain in activated T cells (By similarity). Receptor for both classical and non-classical MHC class I molecules (PubMed:16177084). Receptor or ligand for TNF superfamily member TNFRSF14, participating in bidirectional cell-cell contact signaling between antigen presenting cells and lymphocytes. Upon ligation of TNFRSF14, provides stimulatory signal to NK cells enhancing IFNG production and anti-tumor immune response (PubMed:25711213). On activated CD4+ T cells, interacts with TNFRSF14 and downregulates CD28 costimulatory signaling, restricting memory and alloantigen-specific immune response (By similarity). In the context of bacterial infection, acts as a ligand for TNFRSF14 on epithelial cells, triggering the production of antimicrobial proteins and proinflammatory cytokines (PubMed:22801499).[UniProtKB/Swiss-Prot Function] shRNA Design: These shRNA constructs were designed against multiple splice variants at this gene locus. -
The TNF and TNF Receptor Review Superfamilies: Integrating Mammalian Biology
Cell, Vol. 104, 487±501, February 23, 2001, Copyright 2001 by Cell Press The TNF and TNF Receptor Review Superfamilies: Integrating Mammalian Biology Richard M. Locksley,*²³k Nigel Killeen,²k The receptors and ligands in this superfamily have and Michael J. Lenardo§k unique structural attributes that couple them directly to *Department of Medicine signaling pathways for cell proliferation, survival, and ² Department of Microbiology and Immunology differentiation. Thus, they have assumed prominent ³ Howard Hughes Medical Institute roles in the generation of tissues and transient microen- University of California, San Francisco vironments. Most TNF/TNFR SFPs are expressed in the San Francisco, California 94143 immune system, where their rapid and potent signaling § Laboratory of Immunology capabilities are crucial in coordinating the proliferation National Institute of Allergy and Infectious Diseases and protective functions of pathogen-reactive cells. National Institutes of Health Here, we review the organization of the TNF/TNFR SF Bethesda, Maryland 20892 and how these proteins have been adapted for pro- cesses as seemingly disparate as host defense and or- ganogenesis. In interpreting this large and highly active Introduction area of research, we have focused on common themes that unite the actions of these genes in different tissues. Three decades ago, lymphotoxin (LT) and tumor necro- We also discuss the evolutionary success of this super- sis factor (TNF) were identified as products of lympho- familyÐsuccess that we infer from its expansion across cytes and macrophages that caused the lysis of certain the mammalian genome and from its many indispens- types of cells, especially tumor cells (Granger et al., able roles in mammalian biology. -
Imm Catalog.Pdf
$ Gene Symbol A B 3 C 4 D 9 E 10 F 11 G 12 H 13 I 14 J. K 17 L 18 M 19 N 20 O. P 22 R 26 S 27 T 30 U 32 V. W. X. Y. Z 33 A ® ® Gene Symbol Gene ID Antibody Monoclonal Antibody Polyclonal MaxPab Full-length Protein Partial-length Protein Antibody Pair KIt siRNA/Chimera Gene Symbol Gene ID Antibody Monoclonal Antibody Polyclonal MaxPab Full-length Protein Partial-length Protein Antibody Pair KIt siRNA/Chimera A1CF 29974 ● ● ADAMTS13 11093 ● ● ● ● ● A2M 2 ● ● ● ● ● ● ADAMTS20 80070 ● AACS 65985 ● ● ● ADAMTS5 11096 ● ● ● AANAT 15 ● ● ADAMTS8 11095 ● ● ● ● AATF 26574 ● ● ● ● ● ADAMTSL2 9719 ● AATK 9625 ● ● ● ● ADAMTSL4 54507 ● ● ABCA1 19 ● ● ● ● ● ADAR 103 ● ● ABCA5 23461 ● ● ADARB1 104 ● ● ● ● ABCA7 10347 ● ADARB2 105 ● ABCB9 23457 ● ● ● ● ● ADAT1 23536 ● ● ABCC4 10257 ● ● ● ● ADAT2 134637 ● ● ABCC5 10057 ● ● ● ● ● ADAT3 113179 ● ● ● ABCC8 6833 ● ● ● ● ADCY10 55811 ● ● ABCD2 225 ● ADD1 118 ● ● ● ● ● ● ABCD4 5826 ● ● ● ADD3 120 ● ● ● ABCG1 9619 ● ● ● ● ● ADH5 128 ● ● ● ● ● ● ABL1 25 ● ● ADIPOQ 9370 ● ● ● ● ● ABL2 27 ● ● ● ● ● ADK 132 ● ● ● ● ● ABO 28 ● ● ADM 133 ● ● ● ABP1 26 ● ● ● ● ● ADNP 23394 ● ● ● ● ABR 29 ● ● ● ● ● ADORA1 134 ● ● ACAA2 10449 ● ● ● ● ADORA2A 135 ● ● ● ● ● ● ● ACAN 176 ● ● ● ● ● ● ADORA2B 136 ● ● ACE 1636 ● ● ● ● ADRA1A 148 ● ● ● ● ACE2 59272 ● ● ADRA1B 147 ● ● ACER2 340485 ● ADRA2A 150 ● ● ACHE 43 ● ● ● ● ● ● ADRB1 153 ● ● ACIN1 22985 ● ● ● ADRB2 154 ● ● ● ● ● ACOX1 51 ● ● ● ● ● ADRB3 155 ● ● ● ● ACP5 54 ● ● ● ● ● ● ● ADRBK1 156 ● ● ● ● ACSF2 80221 ● ● ADRM1 11047 ● ● ● ● ACSF3 197322 ● ● AEBP1 165 ● ● ● ● ACSL4 2182 ● -
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. -
Expression Tissue
The Journal of Immunology Killer Cell Ig-Like Receptor and Leukocyte Ig-Like Receptor Transgenic Mice Exhibit Tissue- and Cell-Specific Transgene Expression1 Danny Belkin,* Michaela Torkar,* Chiwen Chang,* Roland Barten,* Mauro Tolaini,† Anja Haude,* Rachel Allen,* Michael J. Wilson,* Dimitris Kioussis,† and John Trowsdale2* To generate an experimental model for exploring the function, expression pattern, and developmental regulation of human Ig-like activating and inhibitory receptors, we have generated transgenic mice using two human genomic clones: 52N12 (a 150-Kb clone encompassing the leukocyte Ig-like receptor (LILR)B1 (ILT2), LILRB4 (ILT3), and LILRA1 (LIR6) genes) and 1060P11 (a 160-Kb clone that contains ten killer cell Ig-like receptor (KIR) genes). Both the KIR and LILR families are encoded within the leukocyte receptor complex, and are involved in immune modulation. We have also produced a novel mAb to LILRA1 to facilitate expression studies. The LILR transgenes were expressed in a similar, but not identical, pattern to that observed in humans: LILRB1 was expressed in B cells, most NK cells, and a small number of T cells; LILRB4 was expressed in a B cell subset; and LILRA1 was found on a ring of cells surrounding B cell areas on spleen sections, consistent with other data showing monocyte/macrophage expression. KIR transgenic mice showed KIR2DL2 expression on a subset of NK cells and T cells, similar to the pattern seen in humans, and expression of KIR2DL4, KIR3DS1, and KIR2DL5 by splenic NK cells. These observations indicate that linked regulatory elements within the genomic clones are sufficient to allow appropriate expression of KIRs in mice, and illustrate that the presence of the natural ligands for these receptors, in the form of human MHC class I proteins, is not necessary for the expression of the KIRs observed in these mice. -
Proteomic and Functional Characterisation of LILRA3: Role In
Proteomic and Functional Characterisation of LILRA3: Role in Inflammation Terry Hung-Yi Lee A thesis submitted in fulfilment of the requirements for the degree of Doctor of Philosophy Faculty of Medicine The University of New South Wales 2014 PLEASE TYPE THE UNIVERSITY OF NEW SOUTH WALES Thosis/Dissertatlon Sh09t Surname or Fam1ly name L l .... f.- First name / 'f (Z (1. 1 Other name/s H "'" ~ - \'I Abbre111at1on lor degree as given in the University calendar. Pt> .fh •I "!.1 '.j 17 J/ 0 School f t. t,...., ..> I <>f lVI e.~, u1 f <J t.r-UJ Faculty: M e. o1; c.• " e Tlrte Pr,te.;) ""l(. (j. f' il ,: ..... d .;" "' u"'"r &- d·er;..c&.L J .<\ ~ l/<.tf. Al: ~ " ' ~ ..... , ...., ~~~"""'" " "'~" Abstract 350 word s ma•imum: (PLEASE TYPE) Se e (f'JicJE' -------- Declaration relating to disposition of project thos tsldissortation I hereby grant to the Un1vers1ty of New South Wales or rts agents the nght to areh1ve and to make avatlabte my theSIS or dissertation '" whole or 1n part 1n the University libranes in all forms of media. now or here after known. subject to the provisions of the Copyright Act 1968 I retain all property nghts such as patent nghts I also retain the right to use in future works (such as artldes or bOOks) all or pan of this thesis or dlssenat1on I also authonse Un1vers1ty Microfilms to use the 350 word abstract of my thesis In Dissertation Abstracts International (this is appticable to doctoral ~~· ~l.A I Po .~.. <j 'I fJs JV VJignatur~ J1 Witness Date The Un1vers1ty recogn•ses that there may be exceptional circumstances requinng restrictions on copying or conditions on use. -
CD2 Molecules Redistribute to the Uropod During T Cell Scanning: Implications for Cellular Activation and Immune Surveillance
CD2 molecules redistribute to the uropod during T cell scanning: Implications for cellular activation and immune surveillance Elena V. Tibaldi*†, Ravi Salgia†‡, and Ellis L. Reinherz*†§ *Laboratory of Immunobiology and ‡Division of Adult Oncology, Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, and †Department of Medicine, Harvard Medical School, Boston, MA 02115 Communicated by Stuart F. Schlossman, Dana-Farber Cancer Institute, Boston, MA, April 9, 2002 (received for review February 14, 2002) Dynamic binding between CD2 and CD58 counter-receptors on op- cells, whereas its counter-receptor CD58 is expressed on a posing cells optimizes immune recognition through stabilization of diverse array of nucleated and non-nucleated cells including cell–cell contact and juxtaposition of surface membranes at a distance APCs and stromal cells (reviewed in refs. 11 and 12). CD2 suitable for T cell receptor–ligand interaction. Digitized time-lapse functions in both T cell adhesion and activation processes (13). Ϸ differential interference contrast and immunofluorescence micros- Of note, the weak affinity of the CD2-CD58 interaction (Kd copy on living cells now show that this binding also induces T cell 1 M) is associated with remarkably fast on and off rates that polarization. Moreover, CD2 can facilitate motility of T cells along foster rapid and extensive exchange between CD2 and CD58 antigen-presenting cells via a movement referred to as scanning. Both partners on opposing cell surfaces (14–16). These biophysical activated CD4 and CD8 T cells are able to scan antigen-presenting cells characteristics are reminiscent of the selectin–ligand interactions surfaces in the absence of cognate antigen. -
Megakaryopoiesis in Dengue Virus Infected K562 Cell Promotes Viral Replication Which Inhibits 2 Endomitosis and Accumulation of ROS Associated with Differentiation
bioRxiv preprint doi: https://doi.org/10.1101/2020.06.25.172544; this version posted June 26, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Title: Megakaryopoiesis in Dengue virus infected K562 cell promotes viral replication which inhibits 2 endomitosis and accumulation of ROS associated with differentiation 3 Jaskaran Kaur *1, Yogita Rawat *1, Vikas Sood 2, Deepak Rathore1, Shrikant K. Kumar1, Niraj K. Kumar1 4 and Sankar Bhattacharyya1 5 1 Translational Health Science and Technology Institute, NCR Biotech Science Cluster, PO Box# 4, 6 Faridabad-Gurgaon expressway, Faridabad, Haryana-121001, India 7 2 Department of Biochemistry, School of Chemical and Life Sciences, Jamia Hamdard (Hamdard 8 University) Hamdard Nagar, New Delhi - 110062, India 9 10 *Equal contribution 11 Email for correspondence: [email protected] 12 13 14 Keywords: Dengue virus replication, Megakaryopoiesis, Reactive oxygen species, Endomitosis 15 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.06.25.172544; this version posted June 26, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 16 Abstract: In the human host blood Monocytes and bone marrow Megakaryocytes are implicated as major 17 sites supporting high replication. The human K562 cell line supports DENV replication and represent 18 Megakaryocyte-Erythrocyte progenitors (MEP), replicating features of in vivo Megakaryopoiesis upon 19 stimulation with Phorbol esters. In this article, we report results that indicate the mutual influence of 20 Megakaryopoiesis and DENV replication on each other, through comparison of PMA-induced 21 differentiation of either mock-infected or DENV-infected K562 cells. -
Autologous T Cells Expressing CD30 Chimeric Antigen Receptors For
Published OnlineFirst August 31, 2016; DOI: 10.1158/1078-0432.CCR-16-1365 Cancer Therapy: Clinical Clinical Cancer Research Autologous T Cells Expressing CD30 Chimeric Antigen Receptors for Relapsed or Refractory Hodgkin Lymphoma: An Open-Label Phase I Trial Chun-Meng Wang1, Zhi-Qiang Wu2,YaoWang3, Ye-Lei Guo3,Han-RenDai3, Xiao-Hui Wang2, Xiang Li2, Ya-Jing Zhang1,Wen-YingZhang1, Mei-Xia Chen1, Yan Zhang1, Kai-Chao Feng1,YangLiu4,Su-XiaLi4, Qing-Ming Yang1, and Wei-Dong Han3 Abstract Purpose: Relapsed or refractory Hodgkin lymphoma is a chal- tolerated, with grade 3 toxicities occurring only in two of 18 lenge for medical oncologists because of poor overall survival. We patients. Of 18 patients, seven achieved partial remission and six aimed to assess the feasibility, safety, and efficacy of CD30- achieved stable disease. An inconsistent response of lymphoma targeting CAR T cells in patients with progressive relapsed or was observed: lymph nodes presented a better response than refractory Hodgkin lymphoma. extranodal lesions and the response of lung lesions seemed to Experimental Design: Patients with relapsed or refractory be relatively poor. Lymphocyte recovery accompanied by an Hodgkin lymphoma received a conditioning chemotherapy fol- increase of circulating CAR T cells (peaking between 3 and 9 days lowed by the CART-30 cell infusion. The level of CAR transgenes after infusion) is a probable indictor of clinical response. Analysis in peripheral blood and biopsied tumor tissues was measured of biopsied tissues by qPCR and immunohistochemistry revealed periodically according to an assigned protocol by quantitative the trafficking of CAR T cells into the targeted sites and reduction PCR (qPCR).