DOCSLIB.ORG

3034.Full.Pdf

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
3034.Full.Pdf Characterization of the CD200 Receptor Family in Mice and Humans and Their Interactions with CD200 This information is current as Gavin J. Wright, Holly Cherwinski, Mildred Foster-Cuevas, of September 28, 2021. Gary Brooke, Michael J. Puklavec, Mike Bigler, Yaoli Song, Maria Jenmalm, Dan Gorman, Terri McClanahan, Man-Ru Liu, Marion H. Brown, Jonathon D. Sedgwick, Joseph H. Phillips and A. Neil Barclay J Immunol 2003; 171:3034-3046; ; Downloaded from doi: 10.4049/jimmunol.171.6.3034 http://www.jimmunol.org/content/171/6/3034 References This article cites 39 articles, 20 of which you can access for free at: http://www.jimmunol.org/ http://www.jimmunol.org/content/171/6/3034.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 28, 2021 • 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 © 2003 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Characterization of the CD200 Receptor Family in Mice and Humans and Their Interactions with CD2001 Gavin J. Wright,2,3* Holly Cherwinski,3† Mildred Foster-Cuevas,* Gary Brooke,* Michael J. Puklavec,* Mike Bigler,† Yaoli Song,† Maria Jenmalm,† Dan Gorman,† Terri McClanahan,† Man-Ru Liu,† Marion H. Brown,* Jonathon D. Sedgwick,† Joseph H. Phillips,3,4† and A. Neil Barclay3,4* CD200 (OX2) is a broadly distributed cell surface glycoprotein that interacts with a structurally related receptor (CD200R) expressed on rodent myeloid cells and is involved in regulation of macrophage function. We report the first characterization of human CD200R (hCD200R) and define its binding characteristics to hCD200. We also report the identification of a closely related gene to hCD200R, designated hCD200RLa, and four mouse CD200R-related genes (termed mCD200RLa-d). CD200, CD200R, and Downloaded from CD200R-related genes were closely linked in humans and mice, suggesting that these genes arose by gene duplication. The distributions of the receptor genes were determined by quantitative RT-PCR, and protein expression was confirmed by a set of novel mAbs. The distribution of mouse and human CD200R was similar, with strongest labeling of macrophages and neutrophils, but also other leukocytes, including monocytes, mast cells, and T lymphocytes. Two mCD200 receptor-like family members, designated mCD200RLa and mCD200RLb, were shown to pair with the activatory adaptor protein, DAP12, suggesting that these receptors would transmit strong activating signals in contrast to the apparent inhibitory signal delivered by triggering the http://www.jimmunol.org/ CD200R. Despite substantial sequence homology with mCD200R, mCD200RLa and mCD200RLb did not bind mCD200, and presently have unknown ligands. The CD200 receptor gene family resembles the signal regulatory proteins and killer Ig-related receptors in having receptor family members with potential activatory and inhibitory functions that may play important roles in immune regulation and balance. Because manipulation of the CD200-CD200R interaction affects the outcome of rodent disease models, targeting of this pathway may have therapeutic utility. The Journal of Immunology, 2003, 171: 3034–3046. ell surface molecules containing Ig-like domains are one activation of macrophages in several tissues and a profound in- of the most abundant protein classes found in mamma- crease in susceptibility to autoimmune disease models affecting the C lian genomes (1), and the systematic characterization of brain and joints. These results indicated that CD200-CD200R in- by guest on September 28, 2021 these proteins expressed on leukocytes has provided many insights teractions are involved in the control of myeloid cellular function into their function. For example, the proteins that initiate intercel- (4). The broad tissue distribution of CD200 and changes in its level lular communication by forming receptor-ligand pairs and their of expression provide a mechanism for locally regulating myeloid ϭ ␮ interactions are typified by low affinities (KD 1–100 M) when cellular activity at appropriate sites, such as inflamed tissue (5, 6). measured in the monomeric state (2). Rat CD200 (OX2) is a The CD200-CD200R regulatory mechanism is an attractive target widely distributed cell surface protein that interacts with a receptor for immunomodulation because its manipulation can induce im- (CD200R) that is highly expressed on myeloid cells. Both proteins mune tolerance and autoimmune diseases. CD200-Fc fusion pro- contain two extracellular Ig-like domains, but the receptor differs teins have been shown to provide beneficial immunomodulatory in that it has a longer cytoplasmic tail containing known signaling effects in models of arthritis and allograft rejection (7, 8). motifs (3). The CD200-deficient mouse had observable alterations In this study, we have identified the homologue of the CD200 in the behavior of myeloid cells in tissues that normally expressed receptor in humans, and show that it is expressed at the surface of CD200. These included both an increase in number and state of myeloid cells and T cells and that it binds CD200. A second related gene was analyzed in humans and an additional four genes in mice that we have designated CD200 receptor-like (CD200RL)5 proteins. *Sir William Dunn School of Pathology, University of Oxford, Oxford, United King- Two of the mouse gene products were shown to pair with the immu- † dom; and DNAX Research Institute, Palo Alto, CA 94304 noreceptor tyrosine-based activation motif-containing adapter protein, Received for publication April 14, 2003. Accepted for publication July 9, 2003. DAP12, creating the potential for activating signal transduction. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Materials and Methods 1 This work was supported by the Medical Research Council. DNAX is supported by Cell lines and staining reagents Schering Plough. Human mast cells were derived from freshly isolated cord blood, as pre- 2 Current address: Wellcome Trust Sanger Institute, Genome Campus, Hinxton, Cam- viously described (9, 10). Mouse C57BL/6 mast cells were derived from bridge CB10 1SA, U.K. bone marrow of 2- to 3-wk-old mice. Bone marrow cells were cultured in 3 G.J.W., H.C., J.H.P., and A.N.B. contributed equally to this study. DMEM (BioWhittaker, Walkersville, MD) supplemented with 10% FCS 4 Address correspondence and reprint requests to Dr. A. Neil Barclay, Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, U.K. E-mail address: [email protected], or Dr. Joseph H. Phillips, 5 Abbreviations used in this paper: CD200RL, CD200 receptor-like; EAE, experi- DNAX Research, 901 California Avenue, Palo Alto, CA 94304-1104. E-mail address: mental autoimmune encephalomyelitis; h, human; m, mouse; RU, response unit; EST, [email protected] expressed sequence tag. Copyright © 2003 by The American Association of Immunologists, Inc. 0022-1767/03/$02.00 The Journal of Immunology 3035 (HyClone, Logan, UT), 1.0 mM sodium pyruvate, 0.1 mM nonessential Analysis of the human and mouse genomes amino acids, 0.3 mg/ml of L-glutamine, 20 mM HEPES, 50 ␮M 2-ME, 50 ng/ml of recombinant stem cell factors (PeproTech, Rocky Hill, NJ), and The NCBI human and mouse genome databases were searched using 30 ng/ml of murine rIL-3. After 2 wk, the cells were cultured in RPMI BLAST (12), and corresponding genes and related genes were identified. 1640 medium containing the same supplements as above minus the stem Ability of CD200RL proteins to pair with DAP12 cell factor, but with the addition of 5 ng/ml of murine rIL-4. Ba/F3, a pro-B cell line, was kindly provided by T. Kitamura (University of Tokyo, To- cDNAs encoding full-length hCD200RLa, mCD200RLa, and kyo, Japan). A cDNA containing the CD8 leader segment followed by the mCD200RLb were subcloned into the pMX-pie retrovirus expression vec- FLAG peptide epitope and joined to the extracellular, transmembrane, and tor. Plasmid DNAs representing the various genes were transfected into the cytoplasmic domains of mouse DAP12 (mDAP12) was subcloned into the Phoenix ecotropic virus packaging cell line (G. Nolan), and the viruses retroviral vector pMX-neo (11). Plasmid DNA of this construct was trans- subsequently obtained were used to infect Ba/F3-mDAP12 cells, as previ- fected into the Pheonix ecotropic virus packaging cell line (G. Nolan, Stan- ously described (11). In the absence of a pairing partner, FLAG-tagged ford University, Stanford, CA), and viruses obtained were used to infect DAP12 remains within the cytoplasm of Ba/F3-mDAP12; however, if the Ba/F3 cells. Ba/F3-mDAP12 cells stably express cytoplasmic FLAG- CD200RL proteins can pair with DAP12, the FLAG epitope will appear on tagged mDAP12. Mouse and human peripheral blood leukocytes were pre- the cell surface of Ba/F3-mDAP12. After 1–2 wk in selection conditions, pared from peripheral blood by hypotonic lysis of RBC. Mouse splenic the Ba/F3-mDAP12 cells infected with the various CD200RL genes were leukocytes were prepared from single cell suspensions after hypotonic lysis analyzed by flow cytometry for the surface expression of the FLAG epitope of RBC. of DAP12 (anti-M2 Ab; Sigma-Aldrich, St.
Load more

Recommended publications
  • 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
    [Show full text]
  • 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]
  • CD200 and Its Receptor, CD200R, Modulate Bone Mass Via the Differentiation of Osteoclasts
    CD200 and its receptor, CD200R, modulate bone mass via the differentiation of osteoclasts Weiguo Cui*†, Esteban Cuartas*, Juan Ke*‡, Qing Zhang*, Halldor B. Einarsson*, Jonathon D. Sedgwick§¶, Jun Liʈ, and Agne` s Vignery*,** *Department of Orthopedics and Rehabilitation, Yale School of Medicine, 310 Cedar Street, New Haven, CT 06510; §Schering–Plough Biopharma (DNAX), Palo Alto, CA 94304; and ʈDepartment of Immunology and Inflammation, Boehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, CT 06877 Edited by Richard A. Flavell, Yale University School of Medicine, New Haven, CT, and approved July 25, 2007 (received for review April 11, 2007) Fusion of macrophages is an essential step in the differentiation of plays a role in the recognition of self and in the fusion of macro- osteoclasts, which play a central role in the development and remod- phages (10). To gain further insight into the mechanism of mac- eling of bone. Osteoclasts are important mediators of bone loss, rophage fusion, we subjected fusing alveolar macrophages from rats which leads, for example, to osteoporosis. Macrophage fusion recep- to genome-wide oligonucleotide microarray analysis, and we dis- tor/signal regulatory protein ␣ (MFR/SIRP␣) and its ligand CD47, covered the expression of CD200 de novo at the onset of fusion. which are members of the Ig superfamily (IgSF), have been implicated CD200 also belongs to the IgSF and has a short cytoplasmic tail. in the fusion of macrophages. We show that CD200, which is not It is expressed on various types of mouse and human cells (see ref. expressed in cells that belong to the myeloid lineage, is strongly 11 for a review) and on mouse osteoblasts (12), but not on expressed in macrophages at the onset of fusion.
    [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]
  • A New Insight Into Viral Proteins As Immunomodulatory Therapeutic Agents
    Iranian Journal of Basic Medical Sciences ijbms.mums.ac.ir A new insight into viral proteins as Immunomodulatory therapeutic agents. KSHV vOX2 a homolog of human CD200 as a potent anti-inflammatory protein Maryam Mousavinezhad-Moghaddam 1, Abbas Ali Amin 2, Houshang Rafatpanah 3, Seyed Abdol Rahim Rezaee 4 * 1 Department of Physiology, Biology Division, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran 2 Department of Immunology, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran 3 Immunology Research Centre, Bu-Ali Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran 4 Inflammation and Inflammatory Diseases Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran A R T I C L E I N F O A B S T R A C T Article type: Review article The physiologic function of the immune system is defence against infectious microbes and tumour Article history: cells, Therefore, need to have precise modulatory mechanisms to maintain the body homeostasis. The Received: Aug 12, 2014 mammalian cellular CD200 (OX2)/CD200R interaction is one of such modulatory mechanisms in which Accepted: Nov 13, 2014 myeloid and lymphoid cells are regulated. CD200 and CD200R molecules are membrane proteins that Keywords: their immunomodulatory effects are able to suppress inflammatory responses, particularly in the CD200 privilege sites such as CNS and eyes. Kaposi’s sarcoma-associated herpesvirus (KSHV), encodes a wide Immune modulation variety of immunoregulatory proteins which play central roles in modulating inflammatory and anti- KSHV inflammatory responses in favour of virus dissemination. One such protein is a homologue of the RGD human CD200, encoded by open reading frame (ORF) K14 and therefore called vOX2/vCD200.
    [Show full text]
  • Review Article the Modulatory Effects of Mesenchymal Stem Cells on Osteoclastogenesis
    Hindawi Publishing Corporation Stem Cells International Volume 2016, Article ID 1908365, 13 pages http://dx.doi.org/10.1155/2016/1908365 Review Article The Modulatory Effects of Mesenchymal Stem Cells on Osteoclastogenesis Wessam E. Sharaf-Eldin,1,2 Nourhan Abu-Shahba,2,3 Marwa Mahmoud,1,2,3 and Nagwa El-Badri1 1 Center of Excellence of Stem Cells and Regenerative Medicine, Zewail City of Science and Technology, Sheikh Zayed District, 6thofOctoberCity,Giza12566,Egypt 2Medical Molecular Genetics Department, Human Genetics and Genome Research Division, National Research Centre, Cairo 12411, Egypt 3Stem Cells Research Group, Centre of Excellence for Advanced Sciences, National Research Centre, Cairo 12411, Egypt Correspondence should be addressed to Nagwa El-Badri; [email protected] Received 12 July 2015; Accepted 21 September 2015 AcademicEditor:JoelC.Glover Copyright © 2016 Wessam E. Sharaf-Eldin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The effect of mesenchymal stem cells (MSCs) on bone formation has been extensively demonstrated through several in vitro and in vivo studies. However, few studies addressed the effect of MSCs on osteoclastogenesis and bone resorption. Under physiological conditions, MSCs support osteoclastogenesis through producing the main osteoclastogenic cytokines, RANKL and M-CSF. However, during inflammation, MSCs suppress osteoclast formation and activity, partly via secretion of the key anti- osteoclastogenic factor, osteoprotegerin (OPG). In vitro, co-culture of MSCs with osteoclasts in the presence of high concentrations of osteoclast-inducing factors might reflect the in vivo inflammatory pathology and prompt MSCs to exert an osteoclastogenic suppressive effect.
    [Show full text]
  • Molecular Analyses of Malignant Pleural Mesothelioma
    Molecular Analyses of Malignant Pleural Mesothelioma Shir Kiong Lo National Heart and Lung Institute Imperial College Dovehouse Street London SW3 6LY A thesis submitted for MD (Res) Faculty of Medicine, Imperial College London 2016 1 Abstract Malignant pleural mesothelioma (MPM) is an aggressive cancer that is strongly associated with asbestos exposure. Majority of patients with MPM present with advanced disease and the treatment paradigm mainly involves palliative chemotherapy and best supportive care. The current chemotherapy options are limited and ineffective hence there is an urgent need to improve patient outcomes. This requires better understanding of the genetic alterations driving MPM to improve diagnostic, prognostic and therapeutic strategies. This research aims to gain further insights in the pathogenesis of MPM by exploring the tumour transcriptional and mutational profiles. We compared gene expression profiles of 25 MPM tumours and 5 non-malignant pleura. This revealed differentially expressed genes involved in cell migration, invasion, cell cycle and the immune system that contribute to the malignant phenotype of MPM. We then constructed MPM-associated co-expression networks using weighted gene correlation network analysis to identify clusters of highly correlated genes. These identified three distinct molecular subtypes of MPM associated with genes involved in WNT and TGF-ß signalling pathways. Our results also revealed genes involved in cell cycle control especially the mitotic phase correlated significantly with poor prognosis. Through exome analysis of seven paired tumour/blood and 29 tumour samples, we identified frequent mutations in BAP1 and NF2. Additionally, the mutational profile of MPM is enriched with genes encoding FAK, MAPK and WNT signalling pathways.
    [Show full text]
  • CD200 in Hematological Malignancies: Just a Diagnostic Tool Or More?
    Editorial Page 1 of 4 CD200 in hematological malignancies: just a diagnostic tool or more? Daniela Damiani, Mario Tiribelli Division of Hematology and Stem Cell Transplantation, Department of Medical Area, Azienda Sanitaria Universitaria Integrata di Udine, Udine, Italy Correspondence to: Prof. Daniela Damiani. Division of Hematology and Stem Cell Transplantation Department of Medical Area, Azienda Sanitaria Universitaria Integrata di Udine, 33100 Udine, Italy. Email: [email protected]. Provenance: This is a Guest Editorial commissioned by the Section Editor Baohong Yue (Hematology lab in Department of Clinical Laboratory Medicine, The First Affiliated Hospital, College of Medicine, Zhengzhou University, Zhengzhou, China). Comment on: Sandes AF, de Lourdes Chauffaille M, Oliveira CR, et al. CD200 has an important role in the differential diagnosis of mature B cell neoplasms by multiparameter flow cytometry. Cytometry B Clin Cytom 2014;86:98-105. Received: 28 July 2017; Accepted: 08 August 2017; Published: 15 September 2017. doi: 10.21037/jlpm.2017.08.08 View this article at: http://dx.doi.org/10.21037/jlpm.2017.08.08 Over the past two decades, the increased number of monoclonal Cytometry, Sandes and colleagues tested the diagnostic antibodies and the constantly expanding availability of utility of CD200 in differential diagnosis of 159 patients fluorescence probes significantly improved the efficiency with mature B lymphoproliferative diseases (3). They and the accuracy of flow cytometric analysis, providing not only added CD200 to a conventional MFC panel, relevant information for the diagnosis, classification and evaluating its dichotomous expression, but also compared follow up of various hematological malignancies. As a the fluorescence intensity in the tested cases, with the aim to diagnostic tool, together with morphology and molecular create a reference pool of CD200 expression intensity that genetics, flow cytometry has become a gold standard in may further discriminate within the CD200-positive group.
    [Show full text]
  • Cell Surface Marker Profiling of Human Tracheal Basal Cells Reveals Distinct
    Respiratory Research This Provisional PDF corresponds to the article as it appeared upon acceptance. Fully formatted PDF and full text (HTML) versions will be made available soon. Cell surface marker profiling of human tracheal basal cells reveals distinct subpopulations, identifies MST1/MSP as a mitogenic signal, and identifies new biomarkers for lung squamous cell carcinomas Respiratory Research (2014)15:1513Sample doi:10.1186/s12931-014-0160-8 Emily Van de Laar ([email protected]) Monica Clifford ([email protected]) Stefan Hasenoeder ([email protected]) Bo Ram Kim ([email protected]) Dennis Wang ([email protected]) Sharon Lee ([email protected]) Josh Paterson ([email protected]) Nancy M Vu ([email protected]) Thomas K Waddell ([email protected]) Shaf Keshavjee ([email protected]) Ming-Sound Tsao ([email protected]) Laurie Ailles ([email protected]) Nadeem Moghal ([email protected]) Sample ISSN 1465-9921 Article type Research Submission date 26 November 2013 Acceptance date 17 December 2014 Article URL http://dx.doi.org/10.1186/s12931-014-0160-8 Like all articles in BMC journals, this peer-reviewed article can be downloaded, printed and distributed freely for any purposes (see copyright notice below). Articles in BMC journals are listed in PubMed and archived at PubMed Central. For information about publishing your research in BMC journals or any BioMed Central journal, go to http://www.biomedcentral.com/info/authors/ © 2014 Van de Laar et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.
    [Show full text]
  • Single-Cell Transcriptome Profiling of the Kidney Glomerulus Identifies Key Cell Types and Reactions to Injury
    BASIC RESEARCH www.jasn.org Single-Cell Transcriptome Profiling of the Kidney Glomerulus Identifies Key Cell Types and Reactions to Injury Jun-Jae Chung ,1 Leonard Goldstein ,2 Ying-Jiun J. Chen,2 Jiyeon Lee ,1 Joshua D. Webster,3 Merone Roose-Girma,2 Sharad C. Paudyal,4 Zora Modrusan,2 Anwesha Dey,5 and Andrey S. Shaw1 Due to the number of contributing authors, the affiliations are listed at the end of this article. ABSTRACT Background The glomerulus is a specialized capillary bed that is involved in urine production and BP control. Glomerular injury is a major cause of CKD, which is epidemic and without therapeutic options. Single-cell transcriptomics has radically improved our ability to characterize complex organs, such as the kidney. Cells of the glomerulus, however, have been largely underrepresented in previous single-cell kidney studies due to their paucity and intractability. Methods Single-cell RNA sequencing comprehensively characterized the types of cells in the glomerulus from healthy mice and from four different disease models (nephrotoxic serum nephritis, diabetes, doxo- rubicin toxicity, and CD2AP deficiency). Results Allcelltypesintheglomeruluswereidentified using unsupervised clustering analysis. Novel marker genes and gene signatures of mesangial cells, vascular smooth muscle cells of the afferent and efferent arteri- oles, parietal epithelial cells, and three types of endothelial cells were identified. Analysis of the disease models revealed cell type–specific and injury type–specific responses in the glomerulus, including acute activation of the Hippo pathway in podocytes after nephrotoxic immune injury. Conditional deletion of YAP or TAZ resulted in more severe and prolonged proteinuria in response to injury, as well as worse glomerulosclerosis.
    [Show full text]
  • CD200 Restrains Macrophage Attack on Oligodendrocyte Precursors Via Toll-Like Receptor 4 Downregulation
    CD200 restrains macrophage attack on oligodendrocyte precursors via toll-like receptor 4 downregulation The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Hayakawa, Kazuhide, Loc-Duyen D Pham, Ji Hae Seo, Nobukazu Miyamoto, Takakuni Maki, Yasukazu Terasaki, Sava Sakadzic, et al. 2016. “CD200 Restrains Macrophage Attack on Oligodendrocyte Precursors via Toll-Like Receptor 4 Downregulation.” Journal of Cerebral Blood Flow & Metabolism 36 (4) (April): 781–793. doi:10.1177/0271678x15606148. Published Version 10.1177/0271678X15606148 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:32741920 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Open Access Policy Articles, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#OAP Page 1 of 31 Journal of Cerebral Blood Flow and Metabolism 1 2 3 4 Resubmission of JCBFM-0361-15-ORIG by Hayakawa et al. 5 6 7 Dear Drs. Dirnagl and Lauritzen, 8 9 Confidential: For Review Only 10 My colleagues and I are grateful for all the very helpful comments from all reviewers. Basically, we agree and 11 have tried to incorporate all these important suggestions into our revised paper. Point-by-point responses are 12 13 listed below. 14 15 16 Reviewer 1 17 18 19 1. There are some mistakes. In the Abstract and Materials and Methods, the authors stated that; “Treatment 20 β 21 with CD200-Fc upregulated alternatively activated macrophage markers such as Arg1, TGM2, and TGF- , in 22 part via enhanced C/EBP-beta transcriptional pathways”.
    [Show full text]
  • BMP-IHH-Mediated Interplay Between Mesenchymal Stem Cells and Osteoclasts Supports Calvarial Bone Homeostasis and Repair
    Bone Research www.nature.com/boneres ARTICLE OPEN BMP-IHH-mediated interplay between mesenchymal stem cells and osteoclasts supports calvarial bone homeostasis and repair Yuxing Guo1,2, Yuan Yuan1, Ling Wu3, Thach-Vu Ho1, Junjun Jing1,4, Hideki Sugii1,5, Jingyuan Li1, Xia Han1, Jifan Feng1, Chuanbin Guo2 and Yang Chai1 Calvarial bones are connected by fibrous sutures. These sutures provide a niche environment that includes mesenchymal stem cells (MSCs), osteoblasts, and osteoclasts, which help maintain calvarial bone homeostasis and repair. Abnormal function of osteogenic cells or diminished MSCs within the cranial suture can lead to skull defects, such as craniosynostosis. Despite the important function of each of these cell types within the cranial suture, we have limited knowledge about the role that crosstalk between them may play in regulating calvarial bone homeostasis and injury repair. Here we show that suture MSCs give rise to osteoprogenitors that show active bone morphogenetic protein (BMP) signalling and depend on BMP-mediated Indian hedgehog (IHH) signalling to balance osteogenesis and osteoclastogenesis activity. IHH signalling and receptor activator of nuclear factor kappa-Β ligand (RANKL) may function synergistically to promote the differentiation and resorption activity of osteoclasts. Loss of Bmpr1a in MSCs leads to downregulation of hedgehog (Hh) signalling and diminished cranial sutures. Significantly, activation of Hh signalling partially restores suture morphology in Bmpr1a mutant mice, suggesting the functional importance of BMP-mediated Hh signalling in regulating suture tissue homeostasis. Furthermore, there is an increased number of CD200+ cells in Bmpr1a mutant mice, which may also contribute to the inhibited osteoclast activity in the sutures of mutant mice.
    [Show full text]