DOCSLIB.ORG

Terminal Effector CD8 T Cells Defined by an IKZF2+IL-7R

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Terminal Effector CD8 T Cells Defined by an IKZF2+IL-7R Terminal Effector CD8 T Cells Defined by an IKZF2 +IL-7R− Transcriptional Signature Express Fc γRIIIA, Expand in HIV Infection, and Mediate Potent HIV-Specific This information is current as Antibody-Dependent Cellular Cytotoxicity of September 23, 2021. Prossy Naluyima, Kerri G. Lal, Margaret C. Costanzo, Gustavo H. Kijak, Veronica D. Gonzalez, Kim Blom, Leigh Anne Eller, Matthew Creegan, Ting Hong, Dohoon Kim, Thomas C. Quinn, Niklas K. Björkström, Hans-Gustaf Downloaded from Ljunggren, David Serwadda, Elly T. Katabira, Nelson K. Sewankambo, Ronald H. Gray, Jared M. Baeten, Nelson L. Michael, Fred Wabwire-Mangen, Merlin L. Robb, Diane L. Bolton, Johan K. Sandberg and Michael A. Eller J Immunol published online 13 September 2019 http://www.jimmunol.org/ http://www.jimmunol.org/content/early/2019/09/12/jimmun ol.1900422 Supplementary http://www.jimmunol.org/content/suppl/2019/09/12/jimmunol.190042 Material 2.DCSupplemental by guest on September 23, 2021 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 *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 Author Choice Freely available online through The Journal of Immunology Author Choice option 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 © 2019 The Authors. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published September 13, 2019, doi:10.4049/jimmunol.1900422 The Journal of Immunology Terminal Effector CD8 T Cells Defined by an IKZF2+IL-7R2 Transcriptional Signature Express FcgRIIIA, Expand in HIV Infection, and Mediate Potent HIV-Specific Antibody-Dependent Cellular Cytotoxicity Prossy Naluyima,*,†,1 Kerri G. Lal,†,‡,x,1 Margaret C. Costanzo,‡,x Gustavo H. Kijak,‡,x Veronica D. Gonzalez,† Kim Blom,† Leigh Anne Eller,‡,x Matthew Creegan,‡,x Ting Hong,{ Dohoon Kim,‡,x Thomas C. Quinn,‖,# Niklas K. Bjo¨rkstro¨m,† Hans-Gustaf Ljunggren,† David Serwadda,** Elly T. Katabira,†† Nelson K. Sewankambo,†† ‡‡ {,xx,{{ ‡ Ronald H. Gray, Jared M. Baeten, Nelson L. Michael, Fred Wabwire-Mangen,* Downloaded from Merlin L. Robb,‡,x Diane L. Bolton,‡,x Johan K. Sandberg,†,2 and Michael A. Eller‡,x,2 HIV-1 infection expands large populations of late-stage differentiated CD8 T cells that may persist long after viral escape from TCR recognition. In this study, we investigated whether such CD8 T cell populations can perform unconventional innate-like antiviral effector functions. Chronic untreated HIV-1 infection was associated with elevated numbers of CD45RA+CD57+ terminal + effector CD8 T cells expressing FcgRIIIA (CD16). The FcgRIIIA CD8 T cells displayed a distinctive transcriptional profile http://www.jimmunol.org/ between conventional CD8 T cells and NK cells, characterized by high levels of IKZF2 and low expression of IL7R. This transcriptional profile translated into a distinct NKp80+ IL-7Ra2 surface phenotype with high expression of the Helios tran- scription factor. Interestingly, the FcgRIIIA+ CD8 T cells mediated HIV-specific Ab-dependent cellular cytotoxicity (ADCC) activity at levels comparable with NK cells on a per cell basis. The FcgRIIIA+ CD8 T cells were highly activated in a manner that correlated positively with expansion of the CD8 T cell compartment and with plasma levels of soluble mediators of antiviral immunity and inflammation such as IP-10, TNF, IL-6, and TNFRII. The frequency of FcgRIIIA+ CD8 T cells persisted as patients initiated suppressive antiretroviral therapy, although their activation levels declined. These data indicate that terminally differ- entiated effector CD8 T cells acquire enhanced innate cell-like characteristics during chronic viral infection and suggest that HIV- by guest on September 23, 2021 specific ADCC is a function CD8 T cells use to target HIV-infected cells. Furthermore, as the FcgRIIIA+ CD8 T cells persist in treatment, they contribute significantly to the ADCC-capable effector cell pool in patients on antiretroviral therapy. The Journal of Immunology, 2019, 203: 000–000. he exquisite sensitivity and specificity of TCR-mediated with initial viral decline; however, the response fails to completely sensing of infection is central to the function of T cells suppress or clear infection (1–4). Since the initial character- T but can also, in some situations, limit their ability to ization of HIV-specific cytotoxic CD8 T cells in the late 1980s provide effective immunity. This is evident in the context of HIV-1 (5–9), the limitations in their ability to control viral replication infection, in which the appearance of HIV-1–specific T cells coincides and clear infection are evident (10, 11). High mutation rates in *Makerere University Walter Reed Project, Kampala, Uganda; †Center for Infectious Received for publication April 11, 2019. Accepted for publication August 20, 2019. Medicine, Department of Medicine, Karolinska Institutet, 17177 Stockholm, Swe- This work was supported by a cooperative agreement (W81XWH-07-2-0067) be- den; ‡U.S. Military HIV Research Program, Walter Reed Army Institute of Research, x tween the Henry M. Jackson Foundation for the Advancement of Military Medicine Silver Spring, MD 20910; Henry M. Jackson Foundation for the Advancement of { and the U.S. Department of Defense and with an Interagency Agreement (1Y-A1-26- Military Medicine, Bethesda, MD 20817; Department of Global Health, University ‖ 42-07) with the Division of AIDS, National Institute of Allergy and Infectious Dis- of Washington School of Public Health, Seattle, WA 98195; Laboratory of Immuno- eases, National Institutes of Health, the Swedish Research Council, the Swedish regulation, Division of Intramural Research, National Institute of Allergy and Infectious Cancer Society, and the Karolinska Institutet. Sample collection for the Couples Diseases, National Institutes of Health, Bethesda, MD 20852; #School of Medicine, Johns Observational Study was supported by the Bill and Melinda Gates Foundation (Grant Hopkins University, Baltimore, MD 21205; **Rakai Health Sciences Program, Uganda 41185). Virus Research Institute, Entebbe, Uganda; ††Faculty of Medicine, Makerere University College of Health Sciences, Kampala, Uganda; ‡‡Bloomberg School of Public Health, Address correspondence and reprint requests to Dr. Michael A. Eller, U.S. Military Johns Hopkins University, Baltimore, MD 21205; xxDepartment of Medicine, University of HIV Research Program, Walter Reed Army Institute of Research, 503 Robert Grant Washington School of Public Health, Seattle, WA 98195; and {{Department of Epidemi- Avenue, 1N11, Silver Spring, MD 20910. E-mail address: [email protected] ology, University of Washington School of Public Health, Seattle, WA 98195 The online version of this article contains supplemental material. 1The two first authors contributed equally and should both be considered first authors. Abbreviations used in this article: ADCC, Ab-dependent cellular cytotoxicity; ART, 2The two last authors contributed equally and should both be considered senior antiretroviral therapy; COS, Couples Observation Study; Eomes, eomesodermin; authors. FDR, false discovery rate; HCV, hepatitis C virus; KIR, killer Ig-like receptor; MFI, mean fluorescence intensity; PCA, principal component analysis. ORCIDs: 0000-0002-8970-0198 (K.G.L.); 0000-0003-2043-1513 (L.A.E.); 0000- 0002-0404-1315 (T.C.Q.); 0000-0002-0967-076X (N.K.B.); 0000-0003-0908- This article is distributed under the terms of the CC BY 4.0 Unported license. 7387 (H.-G.L.); 0000-0001-9362-053X (N.K.S.); 0000-0001-5882-5548 (N.L.M.); 0000-0003-3949-9649 (M.L.R.); 0000-0002-6275-0750 (J.K.S.); 0000-0003-3905- Copyright Ó 2019 The Authors. 4877 (M.A.E.). www.jimmunol.org/cgi/doi/10.4049/jimmunol.1900422 2 TERMINAL EFFECTOR FcgRIIIA+ CD8 T CELLS EXPAND IN HIV HIV-1 contribute to the ability of the virus to escape adaptive Ethics statement T cell responses (3, 12–14). Also, HIV-specific T cells become The study was approved by the following institutional review boards in the functionally impaired during chronic infection, additionally United States and Uganda: the institutional Review Boards of Uganda’s limiting their ability to control viral replication (15–17). Indeed, National Council for Science and Technology and the National AIDS polyfunctional HIV-specific T cell responses are associated with Research Committee, as well as Division of Human Subjects Protection at better disease outcomes compared with those with a narrower the Walter Reed Army Institute of Research. All participants gave written- informed consent, or written-informed consent was obtained from the functional breadth (18–20). In chronic HIV-1 infection, the parent or legal guardian of those aged 17. For samples from the COS in replicating viral quasispecies have, to a large extent, mutated Kampala, Uganda, all participants gave written-informed consent, and away from the originally transmitted viral sequence under T cell ethical approvals for the study were obtained from Uganda’s National selection pressure, and this probably contributes to the accu- Council for Science
Load more

Recommended publications
  • 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.
    [Show full text]
  • Early Detection of Peripheral Blood Cell Signature in Children Developing B-Cell Autoimmunity at a Young Age
    2024 Diabetes Volume 68, October 2019 Early Detection of Peripheral Blood Cell Signature in Children Developing b-Cell Autoimmunity at a Young Age Henna Kallionpää,1 Juhi Somani,2 Soile Tuomela,1 Ubaid Ullah,1 Rafael de Albuquerque,1 Tapio Lönnberg,1 Elina Komsi,1 Heli Siljander,3,4 Jarno Honkanen,3,4 Taina Härkönen,3,4 Aleksandr Peet,5,6 Vallo Tillmann,5,6 Vikash Chandra,3,7 Mahesh Kumar Anagandula,8 Gun Frisk,8 Timo Otonkoski,3,7 Omid Rasool,1 Riikka Lund,1 Harri Lähdesmäki,2 Mikael Knip,3,4,9,10 and Riitta Lahesmaa1 Diabetes 2019;68:2024–2034 | https://doi.org/10.2337/db19-0287 The appearance of type 1 diabetes (T1D)-associated function before T1D and suggest a potential role for IL32 autoantibodies is the first and only measurable param- in the pathogenesis of T1D. eter to predict progression toward T1D in genetically susceptible individuals. However, autoantibodies indi- cate an active autoimmune reaction, wherein the im- Family and sibling studies in type 1 diabetes (T1D) have mune tolerance is already broken. Therefore, there is implicated a firm genetic predisposition to a locus con- a clear and urgent need for new biomarkers that predict taining HLA class I and class II genes on chromosome the onset of the autoimmune reaction preceding auto- 6 suggesting a role for CD4+ as well as CD8+ T cells in T1D fl antibody positivity or re ect progressive b-cell destruc- pathogenesis (1–3). As much as 30–50% of the genetic risk – tion. Here we report the mRNA sequencing based is conferred by HLA class II molecules, which are crucial in analysis of 306 samples including fractionated samples antigen presentation to CD4+ T cells.
    [Show full text]
  • Downloaded the Normalized Gene Expression Profile from the GEO (Package Geoquery (5))
    1 SUPPLEMENTARY MATERIALS 2 Supplementary Methods 3 Study design 4 The workflow to identify and validate the TME risk score and TME subtypes in gastric cancer is 5 depicted in Fig. S1. We first estimated the absolute abundance levels of the major stromal and 6 immune cell types in the TME using bulk gene expression data, and assessed the prognostic 7 effect of these cells in a discovery cohort. Next, we constructed a TME risk score and validated it 8 in two independent gene expression validation cohorts and three immunohistochemistry 9 validation cohorts. Finally, we stratified patients into four TME subtypes and examined their 10 genomic and molecular features and relation to established molecular subtypes. 11 Gene expression data 12 To explore the prognostic landscape of the TME, we used four gene expression profile (GEP) 13 datasets of resected gastric cancer patients with publicly available clinical information, namely, 14 ACRG (GSE62254) (1), GSE15459 (2), GSE84437 (3), and TCGA stomach adenocarcinoma 15 (STAD). Specifically, the raw microarray data in the ACRG cohort and GSE15459 were retrieved 16 from the Gene Expression Omnibus (GEO), and normalized by the RMA algorithm (package affy) 17 using custom chip definition files (Brainarray version 23 (4)) that convert Affymetrix probesets to 18 Entrez gene IDs. For GSE84437 dataset, which was measured by the Illumina platform, we 19 downloaded the normalized gene expression profile from the GEO (package GEOquery (5)). The 20 Illumina probes were also mapped to Entrez genes. For multiple probes mapping to the same 21 Entrez gene, we selected the one with the maximum mean expression level as the surrogate for 22 the Entrez gene using the function of collapseRows (6) (package WGCNA).
    [Show full text]
  • Anti-NCR1 Antibody [29A1.4] (FITC) (ARG23568)
    Product datasheet [email protected] ARG23568 Package: 50 μg anti-NCR1 antibody [29A1.4] (FITC) Store at: 4°C Summary Product Description FITC-conjugated Rat Monoclonal antibody [29A1.4] recognizes NCR1. Rat anti Mouse CD335 antibody, clone 29A1.4 recognizes natural killer cell p46-related protein (NKp46), otherwise known as CD335, which is uniquely expressed by resting and activated natural killer (NK) cells, but no expression of CD335 has been detected on B cells, T cells, monocytes or granulocytes. It is a major NK cell lysis receptor for autologous pathogen-infected and tumor target cells during natural cytotoxicity responses. Ligands of CD335 include viral hemagglutinins (HAs) and heparan sulfate proteoglycans (HSPGs) on the surface of tumor cells. Staining with Rat anti mouse CD335 (29A1.4) is not strain specific and the antibody has been used to stain C57BL/6, SJL, CBA/CA and BALB/c strains. Clone 29A1.4 also activates NK cells in vitro. It does not deplete NK cells in vivo. Tested Reactivity Ms Tested Application FACS Host Rat Clonality Monoclonal Clone 29A1.4 Isotype IgG2a Target Name NCR1 Antigen Species Mouse Immunogen NKP46-IgG1 Fc fusion protein. Conjugation FITC Alternate Names CD antigen CD335; Natural killer cell p46-related protein; Lymphocyte antigen 94 homolog; Natural cytotoxicity triggering receptor 1; hNKp46; NKP46; NKp46; NK cell-activating receptor; LY94; CD335; NK- p46 Application Instructions Application table Application Dilution FACS 1:2 - 1:5 Application Note FACS: Use 10 µl of the suggested working dilution to label 10^6 cells in 100 µl. * The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist.
    [Show full text]
  • 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
    [Show full text]
  • Markers of T Cell Senescence in Humans
    International Journal of Molecular Sciences Review Markers of T Cell Senescence in Humans Weili Xu 1,2 and Anis Larbi 1,2,3,4,5,* 1 Biology of Aging Program and Immunomonitoring Platform, Singapore Immunology Network (SIgN), Agency for Science Technology and Research (A*STAR), Immunos Building, Biopolis, Singapore 138648, Singapore; [email protected] 2 School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore 3 Department of Microbiology, National University of Singapore, Singapore 117597, Singapore 4 Department of Geriatrics, Faculty of Medicine, University of Sherbrooke, Sherbrooke, QC J1K 2R1, Canada 5 Faculty of Sciences, University ElManar, Tunis 1068, Tunisia * Correspondence: [email protected]; Tel.: +65-6407-0412 Received: 31 May 2017; Accepted: 26 July 2017; Published: 10 August 2017 Abstract: Many countries are facing the aging of their population, and many more will face a similar obstacle in the near future, which could be a burden to many healthcare systems. Increased susceptibility to infections, cardiovascular and neurodegenerative disease, cancer as well as reduced efficacy of vaccination are important matters for researchers in the field of aging. As older adults show higher prevalence for a variety of diseases, this also implies higher risk of complications, including nosocomial infections, slower recovery and sequels that may reduce the autonomy and overall quality of life of older adults. The age-related effects on the immune system termed as “immunosenescence” can be exemplified by the reported hypo-responsiveness to influenza vaccination of the elderly. T cells, which belong to the adaptive arm of the immune system, have been extensively studied and the knowledge gathered enables a better understanding of how the immune system may be affected after acute/chronic infections and how this matters in the long run.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Human Β‑1,3‑Glucuronyltransferase 1/B3GAT1 Antibody Monoclonal Mouse Igg2a Clone # 1002707 Catalog Number: MAB8560
    Human β‑1,3‑Glucuronyltransferase 1/B3GAT1 Antibody Monoclonal Mouse IgG2A Clone # 1002707 Catalog Number: MAB8560 DESCRIPTION Species Reactivity Human Specificity Detects human β-1,3-Glucuronyltransferase 1/B3GAT1 in direct ELISAs. Source Monoclonal Mouse IgG2A Clone # 1002707 Purification Protein A or G purified from hybridoma culture supernatant Immunogen Chinese Hamster Ovary cell line, CHO-derived human β‑1,3‑Glucuronyltransferase 1/B3GAT1 His25-Ile334 Accession # Q9P2W7 Formulation Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. See Certificate of Analysis for details. *Small pack size (-SP) is supplied either lyophilized or as a 0.2 μm filtered solution in PBS. APPLICATIONS Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website. Recommended Sample Concentration Immunohistochemistry 5-25 µg/mL See Below DATA Immunohistochemistry β-1,3-Glucuronyltransferase 1/B3GAT1 in Human Brain. β-1,3-Glucuronyltransferase 1/B3GAT1 was detected in immersion fixed paraffin-embedded sections of human brain (cortex) using Mouse Anti-Human β-1,3- Glucuronyltransferase 1/B3GAT1 Monoclonal Antibody (Catalog # MAB8560) at 5 µg/mL for 1 hour at room temperature followed by incubation with the Anti-Mouse IgG VisUCyte™ HRP Polymer Antibody (Catalog # VC001). Before incubation with the primary antibody, tissue was subjected to heat-induced epitope retrieval using Antigen Retrieval Reagent-Basic (Catalog # CTS013). Tissue was stained using DAB (brown) and counterstained with hematoxylin (blue). Specific staining was localized to cytoplasm in neurons. View our protocol for IHC Staining with VisUCyte HRP Polymer Detection Reagents. PREPARATION AND STORAGE Reconstitution Reconstitute at 0.5 mg/mL in sterile PBS.
    [Show full text]
  • Receptor Nkp46 Cells by the NK Β Murine Pancreatic Recognition And
    Recognition and Killing of Human and Murine Pancreatic β Cells by the NK Receptor NKp46 This information is current as Chamutal Gur, Jonatan Enk, Sameer A. Kassem, Yaron of September 27, 2021. Suissa, Judith Magenheim, Miri Stolovich-Rain, Tomer Nir, Hagit Achdout, Benjamin Glaser, James Shapiro, Yaakov Naparstek, Angel Porgador, Yuval Dor and Ofer Mandelboim J Immunol 2011; 187:3096-3103; Prepublished online 17 Downloaded from August 2011; doi: 10.4049/jimmunol.1101269 http://www.jimmunol.org/content/187/6/3096 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2011/08/18/jimmunol.110126 Material 9.DC1 References This article cites 29 articles, 9 of which you can access for free at: http://www.jimmunol.org/content/187/6/3096.full#ref-list-1 Why The JI? Submit online. by guest on September 27, 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 © 2011 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Recognition and Killing of Human and Murine Pancreatic b Cells by the NK Receptor NKp46 Chamutal Gur,*,†,1 Jonatan Enk,*,1 Sameer A.
    [Show full text]
  • Single-Cell Profiling Identifies Impaired Adaptive NK Cells Expanded After HCMV Reactivation in Haploidentical HSCT
    Single-cell profiling identifies impaired adaptive NK cells expanded after HCMV reactivation in haploidentical HSCT Elisa Zaghi, … , Enrico Lugli, Domenico Mavilio JCI Insight. 2021;6(12):e146973. https://doi.org/10.1172/jci.insight.146973. Research Article Hematology Immunology Graphical abstract Find the latest version: https://jci.me/146973/pdf RESEARCH ARTICLE Single-cell profiling identifies impaired adaptive NK cells expanded after HCMV reactivation in haploidentical HSCT Elisa Zaghi,1 Michela Calvi,1,2 Simone Puccio,3 Gianmarco Spata,1 Sara Terzoli,1 Clelia Peano,4 Alessandra Roberto,3 Federica De Paoli,3 Jasper J.P. van Beek,3 Jacopo Mariotti,5 Chiara De Philippis,5 Barbara Sarina,5 Rossana Mineri,6 Stefania Bramanti,5 Armando Santoro,5 Vu Thuy Khanh Le-Trilling,7 Mirko Trilling,7 Emanuela Marcenaro,8 Luca Castagna,5 Clara Di Vito,1,2 Enrico Lugli,3,9 and Domenico Mavilio1,2 1Unit of Clinical and Experimental Immunology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy. 2BIOMETRA, Università degli Studi di Milano, Milan, Italy. 3Laboratory of Translational Immunology, 4Institute of Genetic and Biomedical Research, UoS Milan, National Research Council, and Genomic Unit, 5Bone Marrow Transplant Unit, and 6Molecular Biology Section, Clinical Investigation Laboratory, IRCCS Humanitas Research Hospital, Milan, Italy. 7Institute for Virology, University Hospital Essen, University Duisburg-Essen, Essen, Germany. 8Department of Experimental Medicine, University of Genoa, Genoa, Italy. 9Flow Cytometry Core, IRCCS Humanitas Research Hospital, Milan, Italy. Haploidentical hematopoietic stem cell transplantation (h-HSCT) represents an efficient curative approach for patients affected by hematologic malignancies in which the reduced intensity conditioning induces a state of immunologic tolerance between donor and recipient.
    [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]