CCL17 Production of the Chemokines CCL1 and T Cell Activation Through
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Complementary DNA Microarray Analysis of Chemokines and Their Receptors in Allergic Rhinitis RX Zhang,1 SQ Yu,2 JZ Jiang,3 GJ Liu3
RX Zhang, et al ORIGINAL ARTICLE Complementary DNA Microarray Analysis of Chemokines and Their Receptors in Allergic Rhinitis RX Zhang,1 SQ Yu,2 JZ Jiang,3 GJ Liu3 1 Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai, China 2 Department of Otolaryngology , Jinan General Hospital of PLA, Shandong, China 3 Department of Otolaryngology, Changhai Hospital, Second Military Medical University, Shanghai, China ■ Abstract Objective: To analyze the roles of chemokines and their receptors in the pathogenesis of allergic rhinitis by observing the complementary DNA (cDNA) expression of the chemokines and their receptors in the nasal mucosa of patients with and without allergic rhinitis, using gene chips. Methods: The total RNAs were isolated from the nasal mucosa of 20 allergic rhinitis patients and purifi ed to messenger RNAs, and then reversely transcribed to cDNAs and incorporated with samples of fl uorescence-labeled with Cy5-dUPT (rhinitis patient samples) or Cy3- dUTP (control samples of nonallergic nasal mucosa). Thirty-nine cDNAs of chemokines and their receptors were latticed into expression profi le chips, which were hybridized with probes and then scanned with the computer to study gene expression according to the different fl uorescence intensities. Results: The cDNAs of the following chemokines were upregulated: CCL1, CCL2, CCL5, CCL7, CCL8, CCL11, CCL13, CCL14, CCL17, CCL18, CCL19, CCL24, and CX3CL1 in most of the allergic rhinitis sample chips. CCR2, CCR3, CCR4, CCR5, CCR8 and CX3CR1 were the highly expressed receptor genes. Low expression of CXCL4 was found in these tissues. Conclusion: The T helper cell (TH) immune system is not well regulated in allergic rhinitis. -
Bioinformatics Identification of CCL8/21 As Potential Prognostic
Bioscience Reports (2020) 40 BSR20202042 https://doi.org/10.1042/BSR20202042 Research Article Bioinformatics identification of CCL8/21 as potential prognostic biomarkers in breast cancer microenvironment 1,* 2,* 3 4 5 1 Bowen Chen , Shuyuan Zhang ,QiuyuLi, Shiting Wu ,HanHe and Jinbo Huang Downloaded from http://portlandpress.com/bioscirep/article-pdf/40/11/BSR20202042/897847/bsr-2020-2042.pdf by guest on 28 September 2021 1Department of Breast Disease, Maoming People’s Hospital, Maoming 525000, China; 2Department of Clinical Laboratory, Maoming People’s Hospital, Maoming 525000, China; 3Department of Emergency, Maoming People’s Hospital, Maoming 525000, China; 4Department of Oncology, Maoming People’s Hospital, Maoming 525000, China; 5Department of Medical Imaging, Maoming People’s Hospital, Maoming 525000, China Correspondence: Shuyuan Zhang ([email protected]) Background: Breast cancer (BC) is the most common malignancy among females world- wide. The tumor microenvironment usually prevents effective lymphocyte activation and infiltration, and suppresses infiltrating effector cells, leading to a failure of the host toreject the tumor. CC chemokines play a significant role in inflammation and infection. Methods: In our study, we analyzed the expression and survival data of CC chemokines in patients with BC using several bioinformatics analyses tools. Results: The mRNA expression of CCL2/3/4/5/7/8/11/17/19/20/22 was remark- ably increased while CCL14/21/23/28 was significantly down-regulated in BC tis- sues compared with normal tissues. Methylation could down-regulate expression of CCL2/5/15/17/19/20/22/23/24/25/26/27 in BC. Low expression of CCL3/4/23 was found to be associated with drug resistance in BC. -
Ccl17-Dependent Release of Ccl3 Restrains Regulatory T Cells Thereby Aggravating Atherosclerosis
From the Institute for Cardiovascular Prevention (IPEK) of the Ludwig-Maximilians-Universität München Director: Univ.-Prof. Dr. med. Christian Weber Ccl17-dependent release of Ccl3 restrains regulatory T cells thereby aggravating atherosclerosis Dissertation zum Erwerb des Doctor of Philosophy (Ph.D.) an der Medizinischen Fakultät der Ludwig-Maximilians-Universität München Submitted by M.Sc. Carlos Neideck from Taió in Santa Catarina, Brazil on 21.03.2018 Supervisor: Prof. Dr. med. Christian Weber Second evaluator: Prof. Dr. rer. nat. Jürgen Bernhagen Dean: Prof. Dr. Reinhard Hickel Date of oral defense: 23.07.2018 Affidavit Neideck, Carlos ______________________________________________________________________ Name, Surname ______________________________________________________________________ Street ______________________________________________________________________ Zip Code, Town ______________________________________________________________________ Country I hereby declare, that the submitted thesis entitled: “Ccl17-dependent release of Ccl3 restrains regulatory T cells thereby aggravating atherosclerosis.” is my own work. I have only used the sources indicated and have not made unauthorized use of services of a third party. Where the work of others has been quoted or reproduced, the source is always given. I further declare that the submitted thesis or parts thereof have not been presented as part of an examination degree to any other university. Munich, 25.07.2018 Carlos Neideck Place, date Signature doctoral candidate Confirmation -
Metastasis: Active Lymph Nodes
RESEARCH HIGHLIGHTS METASTASIS subcapsular sinus. Further investiga- tions in vivo revealed that CCR8 acti- vation in tumour cells was required Active lymph nodes for tumour cell extravasation from lymphatic vessels, specifically for the Lymph node metastases are CCL1 activates CCR8-mediated transmigration of tumour cells from indicative of poor prognosis but intracellular signalling in tumour the subcapsular sinus into the lymph tumour cell the mechanisms of tumour cell cells, which resulted in cellular node cortex. entry into the dissemination via the lymphatics changes that are consistent with cell These data unpick the process of are poorly understood. Although it migration. lymphatic dissemination and iden- lymph node is widely believed that tumour cells Is the CCR8–CCL1 paracrine tify the sequence of steps leading to requires active enter the lymph nodes passively with pathway important in lymphatic lymph node metastasis. The authors cell migration the flow of lymph, previous data have metastasis? The suppression of showed that CCR8 is expressed by indicated that some chemokines may CCR8 expression or activity in a large subset of human melanoma promote lymphatic extravasation human melanoma cells did not samples, and it will be interesting and metastasis. Das et al. now dem- affect tumour growth or vasculariz to determine whether this pathway onstrate that tumour cell entry into ation on implantation into immuno can be targeted to prevent lymph the lymph node requires active cell deficient mice, but significantly node metastasis. migration and they also identify the reduced the incidence of lymph Gemma K. Alderton lymphatic endothelium of the lymph node metastasis. Furthermore, ORIGINAL RESEARCH PAPER Das, S. -
Identification of CCL1 As a Gene Differentially Expressed in CD4+ T Cells Expressing TIM-3
http://dx.doi.org/10.4110/in.2011.11.4.203 ORIGINAL ARTICLE pISSN 1598-2629 eISSN 2092-6685 Identification of CCL1 as a Gene Differentially Expressed in CD4+ T cells Expressing TIM-3 Ka Jung Jun1,2, Mi Jin Lee1,2, Dong Chul Shin1,2, Min Yeong Woo1,2, Kyongmin Kim1 and Sun Park1* 1Department of Microbiology and 2Graduate Program of Molecular Medicine, Ajou University School of Medicine, Suwon 442-749, Korea Background: T cell immunoglobulin mucin containing mole- responses and the pathogenesis of several diseases (1). With cule (TIM)-3 is expressed in differentiated Th1 cells and is in- its blocking antibody or its soluble fusion protein TIM-3-Ig, volved in the suppression of the cytokine production by these Th1 immune response as well as anti-tumor immunity is en- cells. However, the regulation of the expression of other T hanced (2-4). Also, induction of tolerance in an experimental cell genes by TIM-3 is unclear. Herein, we attempted to iden- transplantation model is abrogated by injection of TIM-3 anti- tify differentially expressed genes in cells abundantly ex- body (5). Furthermore, dysregulation of T cell TIM-3 ex- pressing TIM-3 compared to cells with low expression of pression is observed in several autoimmune diseases includ- TIM-3. Methods: TIM-3 overexpressing cell clones were es- ing multiple sclerosis, rheumatoid arthritis and Crohn s dis- tablished by transfection of Jurkat T cells with TIM-3 ex- ’ pression vector. For screening of differentially expressed ease (6-8). genes, gene fishing technology based on reverse tran- Galectin-9 and phosphatidylserine have been identified as scription-polymerase chain reaction (RT-PCR) using an an- TIM-3 ligands. -
Identification of Markers Predictive for Response to Induction
Oral Oncology 97 (2019) 56–61 Contents lists available at ScienceDirect Oral Oncology journal homepage: www.elsevier.com/locate/oraloncology Identification of markers predictive for response to induction chemotherapy in patients with sinonasal undifferentiated carcinoma T ⁎ Yoko Takahashia, ,1, Frederico O. Gleber-Nettoa,1, Diana Bellb, Dianna Robertsa, Tong-Xin Xiea, Ahmed S. Abdelmeguida,2, Curtis Pickeringa,Jeffrey N. Myersa, Ehab Y. Hannaa a Department of Head and Neck Surgery, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA b Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA ARTICLE INFO ABSTRACT Keywords: Objectives: Sinonasal undifferentiated carcinoma (SNUC) is a rare, highly aggressive cancer. Despite aggressive Sinonasal undifferentiated carcinoma multimodal therapy, its prognosis remains poor. Because of its locally advanced nature and high propensity for Comprehensive gene expression study distant metastasis, we frequently use induction chemotherapy before definitive therapy in patients with SNUC. Induction chemotherapy However, about 30% of patients do not respond to induction chemotherapy, and lack of response is associated Predictive markers with a poor survival rate. Therefore, in this study, we performed gene expression analysis of SNUC samples to Chemoresistance identify prognostic markers for induction chemotherapy response. Materials and methods: Formalin-fixed, paraffin-embedded SNUC tumor samples from previously untreated pa- tients harvested before induction chemotherapy were used. Gene expression was performed using an oncology gene expression panel. Results: We identified 34 differentially expressed genes that distinguish the responders from the non-responders. Pathway analysis using these genes revealed alteration of multiple pathways between the two groups. Of these 34 genes, 24 distinguished between these two groups. -
Inflammatory Modulation of Hematopoietic Stem Cells by Magnetic Resonance Imaging
Electronic Supplementary Material (ESI) for RSC Advances. This journal is © The Royal Society of Chemistry 2014 Inflammatory modulation of hematopoietic stem cells by Magnetic Resonance Imaging (MRI)-detectable nanoparticles Sezin Aday1,2*, Jose Paiva1,2*, Susana Sousa2, Renata S.M. Gomes3, Susana Pedreiro4, Po-Wah So5, Carolyn Ann Carr6, Lowri Cochlin7, Ana Catarina Gomes2, Artur Paiva4, Lino Ferreira1,2 1CNC-Center for Neurosciences and Cell Biology, University of Coimbra, Coimbra, Portugal, 2Biocant, Biotechnology Innovation Center, Cantanhede, Portugal, 3King’s BHF Centre of Excellence, Cardiovascular Proteomics, King’s College London, London, UK, 4Centro de Histocompatibilidade do Centro, Coimbra, Portugal, 5Department of Neuroimaging, Institute of Psychiatry, King's College London, London, UK, 6Cardiac Metabolism Research Group, Department of Physiology, Anatomy & Genetics, University of Oxford, UK, 7PulseTeq Limited, Chobham, Surrey, UK. *These authors contributed equally to this work. #Correspondence to Lino Ferreira ([email protected]). Experimental Section Preparation and characterization of NP210-PFCE. PLGA (Resomers 502 H; 50:50 lactic acid: glycolic acid) (Boehringer Ingelheim) was covalently conjugated to fluoresceinamine (Sigma- Aldrich) according to a protocol reported elsewhere1. NPs were prepared by dissolving PLGA (100 mg) in a solution of propylene carbonate (5 mL, Sigma). PLGA solution was mixed with perfluoro- 15-crown-5-ether (PFCE) (178 mg) (Fluorochem, UK) dissolved in trifluoroethanol (1 mL, Sigma). This solution was then added to a PVA solution (10 mL, 1% w/v in water) dropwise and stirred for 3 h. The NPs were then transferred to a dialysis membrane and dialysed (MWCO of 50 kDa, Spectrum Labs) against distilled water before freeze-drying. Then, NPs were coated with protamine sulfate (PS). -
Yabe R Et Al, 2014.Pdf
International Immunology, Vol. 27, No. 4, pp. 169–181 © The Japanese Society for Immunology. 2014. All rights reserved. doi:10.1093/intimm/dxu098 For permissions, please e-mail: [email protected] Advance Access publication 25 October 2014 CCR8 regulates contact hypersensitivity by restricting cutaneous dendritic cell migration to the draining lymph nodes Rikio Yabe1,2,3,*, Kenji Shimizu1,2,*, Soichiro Shimizu2, Satoe Azechi2, Byung-Il Choi2, Katsuko Sudo2, Sachiko Kubo1,2, Susumu Nakae2, Harumichi Ishigame2, Shigeru Kakuta4 and Yoichiro Iwakura1,2,3,5 1Center for Animal Disease Models, Research Institute for Biomedical Sciences (RIBS), Tokyo University of Science, Noda, Chiba 278-0022, Japan 2Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, University of Tokyo (IMSUT), Minato-ku, Tokyo 108-8639, Japan 3Medical Mycology Research Center, Chiba University, Inohana Chuo-ku, Chiba 260-8673, Japan RTICLE 4 A Department of Biomedical Science, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, FEATURED Tokyo 113-8657, Japan 5Core Research for Evolutional and Technology (CREST), Japan Science and Technology Agency, Kawaguchi, Saitama 332-0012, Japan Correspondence to: Y. Iwakura; E-mail: [email protected] *These authors equally contributed to this work. Received 2 September 2014, accepted 17 October 2014 Abstract Allergic contact dermatitis (ACD) is a typical occupational disease in industrialized countries. Although various cytokines and chemokines are suggested to be involved in the pathogenesis of ACD, the roles of these molecules remain to be elucidated. CC chemokine receptor 8 (CCR8) is one such molecule, of which expression is up-regulated in inflammatory sites of ACD patients. -
Chemokine Signatures of Pathogen-Specific T Cells II: Memory T Cells in Acute and Chronic Infection
Chemokine Signatures of Pathogen-Specific T Cells II: Memory T Cells in Acute and Chronic Infection This information is current as Bennett Davenport, Jens Eberlein, Tom T. Nguyen, of September 24, 2021. Francisco Victorino, Verena van der Heide, Maxim Kuleshov, Avi Ma'ayan, Ross Kedl and Dirk Homann J Immunol published online 18 September 2020 http://www.jimmunol.org/content/early/2020/09/17/jimmun ol.2000254 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2020/09/17/jimmunol.200025 Material 4.DCSupplemental 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 24, 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 © 2020 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published September 18, 2020, doi:10.4049/jimmunol.2000254 The Journal of Immunology Chemokine Signatures of Pathogen-Specific T Cells II: Memory T Cells in Acute and Chronic Infection Bennett Davenport,*,†,‡,x,{ Jens Eberlein,*,† Tom T. Nguyen,*,‡ Francisco Victorino,*,†,‡ Verena van der Heide,x,{ Maxim Kuleshov,‖,# Avi Ma’ayan,‖,# Ross Kedl,† and Dirk Homann*,†,‡,x,{ Pathogen-specific memory T cells (TM) contribute to enhanced immune protection under conditions of reinfection, and their effective recruitment into a recall response relies, in part, on cues imparted by chemokines that coordinate their spatiotemporal positioning. -
Techniques for Immune Function Analysis Application Handbook 1St Edition
Techniques for Immune Function Analysis Application Handbook 1st Edition BD Biosciences For additional information please access the Immune Function Homepage at www.bdbiosciences.com/immune_function For Research Use Only. Not for use in diagnostic or therapeutic procedures. Purchase does not include or carry any right to resell or transfer this product either as a stand-alone product or as a component of another product. Any use of this product other than the permitted use without the express written authorization of Becton Dickinson and Company is strictly prohibited. All applications are either tested in-house or reported in the literature. See Technical Data Sheets for details. BD, BD Logo and all other trademarks are the property of Becton, Dickinson and Company. ©2003 BD Table of Contents Preface . 4 Chapter 1: Immunofluorescent Staining of Cell Surface Molecules for Flow Cytometric Analysis . 9 Chapter 2: BD™ Cytometric Bead Array (CBA) Multiplexing Assays . 35 Chapter 3: BD™ DimerX MHC:Ig Proteins for the Analysis of Antigen-specific T Cells. 51 Chapter 4: Immunofluorescent Staining of Intracellular Molecules for Flow Cytometric Analysis . 61 Chapter 5: BD FastImmune™ Cytokine Flow Cytometry. 85 Chapter 6: BD™ ELISPOT Assays for Cells That Secrete Biological Response Modifiers . 109 Chapter 7: ELISA for Specifically Measuring the Levels of Cytokines, Chemokines, Inflammatory Mediators and their Receptors . 125 Chapter 8: BD OptEIA™ ELISA Sets and Kits for Quantitation of Analytes in Serum, Plasma, and Cell Culture Supernatants. 143 Chapter 9: BrdU Staining and Multiparameter Flow Cytometric Analysis of the Cell Cycle . 155 Chapter 10: Cell-based Assays for Biological Response Modifiers . 177 Chapter 11: BD RiboQuant™ Multi-Probe RNase Protection Assay System . -
Human CCL15/MIP-1Δ Antibody
Human CCL15/MIP-1δ Antibody Monoclonal Mouse IgG1 Clone # 88119 Catalog Number: MAB3631 DESCRIPTION Species Reactivity Human Specificity Detects human CCL15/MIP1δ in direct ELISAs and Western blots. In direct ELISAs, no crossreactivity with recombinant human CCL1, 2, 3, 4, 5, 7, 8, 11, 13, 14, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, recombinant mouse CCL1, 2, 3, 4, 5, 6, 7, 9, 11, 12, 17, 19, 20, 21, 22, 24, 25, or recombinant rat CCL20 is observed. Source Monoclonal Mouse IgG1 Clone # 88119 Purification Protein A or G purified from ascites Immunogen E. coliderived recombinant human CCL15/MIP1δ Ser46Ile113 Accession # Q16663 Endotoxin Level <0.10 EU per 1 μg of the antibody by the LAL method. 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 Western Blot 1 µg/mL Recombinant Human CCL15/MIP1δ 92 aa (Catalog # 363MG) Neutralization Measured by its ability to neutralize CCL15/MIP1δinduced chemotaxis in the BaF3 mouse proB cell line transfected with human CCR1. The Neutralization Dose (ND50) is typically 520 µg/mL in the presence of 1 ng/mL Recombinant Human CCL15/MIP1δ 68 aa. DATA Neutralization Chemotaxis Induced by CCL15/MIP1δ and Neutral ization by Human CCL15/ MIP1δ Antibody. -
Increased Plasma Levels of the TH2 Chemokine CCL18 Associated With
www.nature.com/scientificreports OPEN Increased Plasma Levels of the TH2 chemokine CCL18 associated with low CD4+ T cell counts in HIV-1- Received: 22 May 2018 Accepted: 25 February 2019 infected Patients with a Suppressed Published: xx xx xxxx Viral Load Prashant Malhotra1, Patrick Haslett2, Barbara Sherry3,4, David H. Shepp1, Paul Barber5, Jonathan Abshier6, Upal Roy6 & Helena Schmidtmayerova7 The chemokine (C-C motif) chemokine ligand 18 (CCL18) is a structural homolog of CCL3 primarily produced by monocyte-derived cells with an M2 phenotype. Elevated levels of CCL18 have been observed in several diseases associated with malignancies and chronic infammation. The role of CCL18 in Human Immunodefciency Virus (HIV-1) infection remains unknown. We analyzed expression levels of T helper cell-mediated (TH2) chemokines CCL18, CCL17, and CCL22 by ELISA in plasma collected from HIV-1-infected and healthy donors. In HIV-1-infected individuals, plasma viral loads were monitored by NucliSense HIV-1 QT assay and T cell counts and expression of the activation marker CD38 were determined by fow cytometry. Our data showed a signifcant increase in plasma levels of CCL18 in HIV-1-infected individuals compared to uninfected controls (p < 0.001) and a signifcant correlation between CCL18 levels and viral load in untreated patients. No signifcant diference of CCL18 levels was detected among the HIV-1-infected patients treated with combined antiretroviral therapy (cART) and HIV-1-untreated patients.CCL18 values are negatively correlated with CD4+CD38+ cell numbers and total CD4+ T cell counts in patients with a suppressed viral load. Notably, plasma levels of the TH2 chemokines CCL17 and CCL22 are also elevated during HIV-1 infection.