DOCSLIB.ORG

B Cell Responses Antiviral Niches by B and Th Cells Augments CXCR5

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
B Cell Responses Antiviral Niches by B and Th Cells Augments CXCR5 CXCR5-Dependent Seeding of Follicular Niches by B and Th Cells Augments Antiviral B Cell Responses This information is current as Tobias Junt, Katja Fink, Reinhold Förster, Beatrice Senn, of October 2, 2021. Martin Lipp, Masamichi Muramatsu, Rolf M. Zinkernagel, Burkhard Ludewig and Hans Hengartner J Immunol 2005; 175:7109-7116; ; doi: 10.4049/jimmunol.175.11.7109 http://www.jimmunol.org/content/175/11/7109 Downloaded from References This article cites 32 articles, 19 of which you can access for free at: http://www.jimmunol.org/content/175/11/7109.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on October 2, 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 © 2005 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology CXCR5-Dependent Seeding of Follicular Niches by B and Th Cells Augments Antiviral B Cell Responses1 Tobias Junt,2* Katja Fink,2* Reinhold Fo¨rster,† Beatrice Senn,3* Martin Lipp,¶ Masamichi Muramatsu,‡ Rolf M. Zinkernagel,* Burkhard Ludewig,2,4§ and Hans Hengartner2* The chemokine receptor CXCR5 and its ligand CXCL13 define the structure of B cell follicles within secondary lymphoid organs. Here, we examined the impact of CXCR5 on antiviral B cell responses in vivo. CXCR5؊/؊ mice showed a normal production of IgM and IgG acutely after infection with vesicular stomatitis virus (VSV) and developed VSV-specific germinal centers. However, impaired Ig class switch and Ab production were observed under conditions of limited availability of Ag (i.e., after immunization with nonreplicating viral particles or soluble Ag). Adoptive transfer of CXCR5-deficient, VSV-specific B and Th cells demon- strated that CXCR5 expression on both B and Th cells is required for an efficient Ig class switch. These experiments revealed that CXCR5 is critical for the coordinated interaction of antiviral T and B cells through its impact on initial B cell expansion and the Downloaded from recruitment of Ag-specific B and Th cells to germinal centers. The Journal of Immunology, 2005, 175: 7109–7116. coordinated interaction of CD4ϩ Th and B cells is cru- We investigated this discrepancy in well characterized viral sys- cial for efficient Ig production (1). The collaboration of tems, by infecting CXCR5Ϫ/Ϫ mice with the cytopathic vesicular Ag-specific Th and B cells in secondary lymphoid or- stomatitis virus (VSV),5 or with the non-cytopathic lymphocytic A Ϫ/Ϫ gans depends on distinct chemokine-chemokine receptor interac- choriomeningitis virus (LCMV), or by immunizing CXCR5 tions, such as CXCR5 and its ligand chemokine CXCL13 (2). mice with nonreplicating VSV-derived Ags (12). The production http://www.jimmunol.org/ CXCL13 is expressed in B cell follicles (3), and CXCR5 is ex- of neutralizing Abs in the acute phase of VSV infection that are pressed by naive B cells and a subpopulation of activated CD4ϩ known to be of high affinity was not impaired in CXCR5Ϫ/Ϫ mice. helper T cells (4). After initial activation in the marginal zone of However, antiviral B cell responses were significantly reduced in the spleen, B cells relocate to the B cell zone through down-reg- CXCR5Ϫ/Ϫ mice under conditions of low antigenic doses. These ulation of S1P1 (5) and then to the border of T and B cell zones impaired B cell responses were caused by the combined effect of through up-regulation of CCR7 (6). After differentiation to plasma CXCR5 deficiency on both Th and B cells. Our results from adop- cells, B cells lose CCR7 and CXCR5 expression and thus leave tive transfer experiments with CXCR5-deficient, VSV-specific Th secondary lymphoid organs (7). CD4ϩ T cells up-regulate CXCR5 and B cells indicate that CXCR5 increases the efficacy of T-de- by guest on October 2, 2021 during activation and localize near B cell follicles (8). These pendent (TD) B cell responses by 1) fostering an efficient Ag- CD4ϩCXCR5ϩ Th cells were shown to enhance the production of specific expansion of B cells in secondary lymphoid organs before IgG and IgA and, to a lesser extent, of IgM in vitro (9, 10) and the Ig class switch and 2) attracting Ag-specific B and Th cells to were thus termed “follicular helper T cells.” Contradictory findings germinal centers (GCs) in the later phase of the immune response. in CXCR5-deficient mice, however, suggested that T-B collabo- ration is not affected by the lack of this chemokine receptor: Materials and Methods Ϫ Ϫ CXCR5 / mice produce normal levels of switched Ig isotypes in Mice vivo after immunization with DNP-keyhole limpet hemocyanin in Ϫ/Ϫ All mice were bred at the Institut fu¨r Labortierkunde (University of Zu¨rich, adiuvant (4), and B cells of CXCR5 mice underwent normal Zu¨rich, Switzerland). B6PLThy1.1 and B6.Cg-IgHaThy1aGpi1a/J (IgH- affinity maturation when 2-phenyl-oxazolone was used as an aThy1.1) mice were obtained originally from The Jackson Laboratory. Ag (11). CXCR5Ϫ/Ϫ mice, nine times backcrossed to 129Sv, were PCR typed as described previously (4). Mice bearing a knock-in construct for the VSV- neutralizing Ab VI10 in their Ig locus (VI10) (13) and TCR-transgenic *Institute of Experimental Immunology, Zu¨rich, Switzerland; †Hannover Medical mice for the T cell-epitope p8 of VSV (L7) (14) have been described Ϫ Ϫ School, Institute of Immunology, Hannover, Germany; ‡Department of Medical previously. Activation-induced deaminase knockout mice (AID / ) (15) Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan; §Research were a gift from S. Fagarasan (Kyoto University, Kyoto, Japan). For adop- Department, Kantonal Hospital St. Gallen, St. Gallen, Switzerland; and ¶Max-Del- tive transfer experiments, VI10 and L7 mice were crossed to CXCR5Ϫ/Ϫ bru¨ck-Center for Molecular Medicine, Berlin, Germany mice that were backcrossed onto the C57BL/6 background for 11 Received for publication March 21, 2005. Accepted for publication September generations. 5, 2005. The costs of publication of this article were defrayed in part by the payment of page Viruses and immunizations charges. This article must therefore be hereby marked advertisement in accordance The LCMV, WE strain, was obtained originally from Dr. F. Lehmann- with 18 U.S.C. Section 1734 solely to indicate this fact. Grube (Heinrich-Pette-Institut, Hamburg, Germany) and propagated as de- 1 This work was supported by the Swiss National Science Foundation and the Kanton scribed previously (16). The VSV, Indiana strain (VSV-IND; of Zu¨rich. Mudd-Summers isolate), was obtained originally from Prof. D. Kolakofsky 2 B.L., H.H., T.J. and K.F. contributed equally to this work. 3 Current address: Intercell AG, Campus Vienna Biocenter 6, A-1030 Vienna, 5 Abbreviations used in this paper: VSV, vesicular stomatitis virus; AID, activation- Austria. induced deaminase; GC, germinal center; LCMV, lymphocytic choriomeningitis vi- 4 Address correspondence and reprint requests to Dr. Burkhard Ludewig, Research rus; VSV-IND, vesicular stomatitis virus, Indiana strain; VSV-G, vesicular stomatitis Department, Kantonsspital St. Gallen, CH-9007 St. Gallen, Switzerland. E-mail ad- virus-glycoprotein; TRITC, tetramethylrhodamine isothiocyanate; PB, permeabiliza- dress: [email protected] tion buffer; TD, T-dependent; TI, T-independent; DC, dendritic cell. Copyright © 2005 by The American Association of Immunologists, Inc. 0022-1767/05/$02.00 7110 CXCR5 IN ANTIVIRAL B CELL RESPONSES (University of Geneva, Geneva, Switzerland). For some experiments, in- washing in PBS, nuclei were counterstained with 4Ј,6Ј-diamino-2-phe- activated VSV-IND was obtained using UV irradiation (7UV 15W; Phil- nylindoledihydrochloride (Sigma-Aldrich), and sections were mounted ips). Recombinant VSV-glycoprotein (VSV-G) was obtained from a cul- with fluorescence mounting solution (DakoCytomation). For histological ture of Spodoptera frugiperda 9 cells after infection with a recombinant detection of CXCL13, acetone-fixed spleen sections were incubated with baculovirus (17). 15 ␮g/ml goat anti-mouse CXCL13, followed by 5 ␮g/ml donkey anti-goat biotin and streptavidin-TRITC. Fluorescence was analyzed under an Olym- Abs and flow cytometry pus UplanApo objective (10ϫ/0.4) with a BX61 fluorescence microscope Abs for flow cytometry and fluorescence microscopy were purchased from (Olympus) and an F-view camera (Soft Imaging System). Single fluores- BD Pharmingen, unless stated otherwise. Streptavidin-tetramethylrhodam- cence channels were acquired with the following Olympus filter sets: Spec- trum orange for TRITC, Spectrum green for FITC, Cy5 for allophycocya- ine isothiocyanate (TRITC) was purchased from Southern Biotechnology Ј Ј Associates. Goat anti-mouse CXCL13 was obtained from R&D Systems, nin, and 4 ,6 -diamino-2-phenylindoledihydrochloride. Color channels and donkey anti-goat IgG was obtained from Jackson ImmunoResearch were assembled automatically with the analySIS software (Soft Imaging Laboratories. The Ab 35.61 specific for a combination of heavy and light System), and images were processed using Adobe Photoshop, without non- chains of the VI10 Ab was produced as described previously (13). Aliquots linear operations, unless stated otherwise. of 5 ϫ 105 cells or three drops of blood were stained in FACS buffer (PBS, 2% FCS, 20 mM EDTA, and 0.03% NaN3) at 4°C for 20 min. Before Results analysis of peripheral blood, erythrocytes were lysed with FACS Lysing Antiviral B cell responses in CXCR5-deficient mice Solution (BD Pharmingen).
Load more

Recommended publications
  • Molecular Signatures of G-Protein-Coupled Receptors A
    REVIEW doi:10.1038/nature11896 Molecular signatures of G-protein-coupled receptors A. J. Venkatakrishnan1, Xavier Deupi2, Guillaume Lebon1,3,4,5, Christopher G. Tate1, Gebhard F. Schertler2,6 & M. Madan Babu1 G-protein-coupled receptors (GPCRs) are physiologically important membrane proteins that sense signalling molecules such as hormones and neurotransmitters, and are the targets of several prescribed drugs. Recent exciting developments are providing unprecedented insights into the structure and function of several medically important GPCRs. Here, through a systematic analysis of high-resolution GPCR structures, we uncover a conserved network of non-covalent contacts that defines the GPCR fold. Furthermore, our comparative analysis reveals characteristic features of ligand binding and conformational changes during receptor activation. A holistic understanding that integrates molecular and systems biology of GPCRs holds promise for new therapeutics and personalized medicine. ignal transduction is a fundamental biological process that is comprehensively, and in the process expand the current frontiers of required to maintain cellular homeostasis and to ensure coordi- GPCR biology. S nated cellular activity in all organisms. Membrane proteins at the In this analysis, we objectively compare known structures and reveal cell surface serve as the communication interface between the cell’s key similarities and differences among diverse GPCRs. We identify a external and internal environments. One of the largest and most diverse consensus structural scaffold of GPCRs that is constituted by a network membrane protein families is the GPCRs, which are encoded by more of non-covalent contacts between residues on the transmembrane (TM) than 800 genes in the human genome1. GPCRs function by detecting a helices.
    [Show full text]
  • Edinburgh Research Explorer
    Edinburgh Research Explorer International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list Citation for published version: Davenport, AP, Alexander, SPH, Sharman, JL, Pawson, AJ, Benson, HE, Monaghan, AE, Liew, WC, Mpamhanga, CP, Bonner, TI, Neubig, RR, Pin, JP, Spedding, M & Harmar, AJ 2013, 'International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands', Pharmacological reviews, vol. 65, no. 3, pp. 967-86. https://doi.org/10.1124/pr.112.007179 Digital Object Identifier (DOI): 10.1124/pr.112.007179 Link: Link to publication record in Edinburgh Research Explorer Document Version: Publisher's PDF, also known as Version of record Published In: Pharmacological reviews Publisher Rights Statement: U.S. Government work not protected by U.S. copyright General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 1521-0081/65/3/967–986$25.00 http://dx.doi.org/10.1124/pr.112.007179 PHARMACOLOGICAL REVIEWS Pharmacol Rev 65:967–986, July 2013 U.S.
    [Show full text]
  • CXCL13/CXCR5 Interaction Facilitates VCAM-1-Dependent Migration in Human Osteosarcoma
    International Journal of Molecular Sciences Article CXCL13/CXCR5 Interaction Facilitates VCAM-1-Dependent Migration in Human Osteosarcoma 1, 2,3,4, 5 6 7 Ju-Fang Liu y, Chiang-Wen Lee y, Chih-Yang Lin , Chia-Chia Chao , Tsung-Ming Chang , Chien-Kuo Han 8, Yuan-Li Huang 8, Yi-Chin Fong 9,10,* and Chih-Hsin Tang 8,11,12,* 1 School of Oral Hygiene, College of Oral Medicine, Taipei Medical University, Taipei City 11031, Taiwan; [email protected] 2 Department of Orthopaedic Surgery, Chang Gung Memorial Hospital, Puzi City, Chiayi County 61363, Taiwan; [email protected] 3 Department of Nursing, Division of Basic Medical Sciences, and Chronic Diseases and Health Promotion Research Center, Chang Gung University of Science and Technology, Puzi City, Chiayi County 61363, Taiwan 4 Research Center for Industry of Human Ecology and Research Center for Chinese Herbal Medicine, Chang Gung University of Science and Technology, Guishan Dist., Taoyuan City 33303, Taiwan 5 School of Medicine, China Medical University, Taichung 40402, Taiwan; [email protected] 6 Department of Respiratory Therapy, Fu Jen Catholic University, New Taipei City 24205, Taiwan; [email protected] 7 School of Medicine, Institute of Physiology, National Yang-Ming University, Taipei City 11221, Taiwan; [email protected] 8 Department of Biotechnology, College of Health Science, Asia University, Taichung 40402, Taiwan; [email protected] (C.-K.H.); [email protected] (Y.-L.H.) 9 Department of Sports Medicine, College of Health Care, China Medical University, Taichung 40402, Taiwan 10 Department of Orthopedic Surgery, China Medical University Beigang Hospital, Yunlin 65152, Taiwan 11 Department of Pharmacology, School of Medicine, China Medical University, Taichung 40402, Taiwan 12 Chinese Medicine Research Center, China Medical University, Taichung 40402, Taiwan * Correspondence: [email protected] (Y.-C.F.); [email protected] (C.-H.T.); Tel.: +886-4-2205-2121-7726 (C.-H.T.); Fax: +886-4-2233-3641 (C.-H.T.) These authors contributed equally to this work.
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • The Unexpected Role of Lymphotoxin Β Receptor Signaling
    Oncogene (2010) 29, 5006–5018 & 2010 Macmillan Publishers Limited All rights reserved 0950-9232/10 www.nature.com/onc REVIEW The unexpected role of lymphotoxin b receptor signaling in carcinogenesis: from lymphoid tissue formation to liver and prostate cancer development MJ Wolf1, GM Seleznik1, N Zeller1,3 and M Heikenwalder1,2 1Department of Pathology, Institute of Neuropathology, University Hospital Zurich, Zurich, Switzerland and 2Institute of Virology, Technische Universita¨tMu¨nchen/Helmholtz Zentrum Mu¨nchen, Munich, Germany The cytokines lymphotoxin (LT) a, b and their receptor genesis. Consequently, the inflammatory microenviron- (LTbR) belong to the tumor necrosis factor (TNF) super- ment was added as the seventh hallmark of cancer family, whose founder—TNFa—was initially discovered (Hanahan and Weinberg, 2000; Colotta et al., 2009). due to its tumor necrotizing activity. LTbR signaling This was ultimately the result of more than 100 years of serves pleiotropic functions including the control of research—indeed—the first observation that tumors lymphoid organ development, support of efficient immune often arise at sites of inflammation was initially reported responses against pathogens due to maintenance of intact in the nineteenth century by Virchow (Balkwill and lymphoid structures, induction of tertiary lymphoid organs, Mantovani, 2001). Today, understanding the underlying liver regeneration or control of lipid homeostasis. Signal- mechanisms of why immune cells can be pro- or anti- ing through LTbR comprises the noncanonical/canonical carcinogenic in different types of tumors and which nuclear factor-jB (NF-jB) pathways thus inducing cellular and molecular inflammatory mediators (for chemokine, cytokine or adhesion molecule expression, cell example, macrophages, lymphocytes, chemokines or proliferation and cell survival.
    [Show full text]
  • Neutrophil Chemoattractant Receptors in Health and Disease: Double-Edged Swords
    Cellular & Molecular Immunology www.nature.com/cmi REVIEW ARTICLE Neutrophil chemoattractant receptors in health and disease: double-edged swords Mieke Metzemaekers1, Mieke Gouwy1 and Paul Proost 1 Neutrophils are frontline cells of the innate immune system. These effector leukocytes are equipped with intriguing antimicrobial machinery and consequently display high cytotoxic potential. Accurate neutrophil recruitment is essential to combat microbes and to restore homeostasis, for inflammation modulation and resolution, wound healing and tissue repair. After fulfilling the appropriate effector functions, however, dampening neutrophil activation and infiltration is crucial to prevent damage to the host. In humans, chemoattractant molecules can be categorized into four biochemical families, i.e., chemotactic lipids, formyl peptides, complement anaphylatoxins and chemokines. They are critically involved in the tight regulation of neutrophil bone marrow storage and egress and in spatial and temporal neutrophil trafficking between organs. Chemoattractants function by activating dedicated heptahelical G protein-coupled receptors (GPCRs). In addition, emerging evidence suggests an important role for atypical chemoattractant receptors (ACKRs) that do not couple to G proteins in fine-tuning neutrophil migratory and functional responses. The expression levels of chemoattractant receptors are dependent on the level of neutrophil maturation and state of activation, with a pivotal modulatory role for the (inflammatory) environment. Here, we provide an overview
    [Show full text]
  • Original Article Expression of Chemokine Receptor CXCR5 in Gastric Cancer and Its Clinical Significance
    Int J Clin Exp Pathol 2016;9(7):7202-7208 www.ijcep.com /ISSN:1936-2625/IJCEP0023559 Original Article Expression of chemokine receptor CXCR5 in gastric cancer and its clinical significance Qing Sun*, Lujun Chen*, Bin Xu, Qi Wang, Xiao Zheng, Peng Du, Dachuan Zhang, Changping Wu, Jingting Jiang Department of Tumor Biological Treatment, The Third Affiliated Hospital, Soochow University, Jiangsu Engineering Research Center for Tumor Immunotherapy, Changzhou, Jiangsu, China. *Equal contributors. Received January 8, 2016; Accepted March 22, 2016; Epub July 1, 2016; Published July 15, 2016 Abstract: The increased expression of chemokine receptor CXCR5 in cancers has been demonstrated. In order to characterize the expression pattern of CXCR5 in cell lines and tissues of gastric cancer and to assess clinical implications, the expression of CXCR5 mRNA in gastric cancer tissues and adjacent tissues was evaluated by real- time RT-PCR. Meanwhile, the expression of CXCR5 in cell lines of human gastric cancer was also analyzed by flow cytometry. Tissue microarray and immunohistochemistry were used to detect the protein expression of CXCR5 in human gastric cancer tissues and adjacent normal tissues. Flow cytometry results revealed the positive expression of CXCR5 in human gastric cancer cell lines such as BGC-823, SGC-7901 and HGC-27 cells. The immunohistochem- istry results showed higher expression of CXCR5 in 52.87% of gastric cancer tissues. The expression of CXCR5 in patients with tumor size less than 2.8 cm subgroup was significantly lower than that in patients with tumor size larger than 2.8 cm subgroup (P = 0.0456). There was no significant correlation between the expression of CXCR5 and other clinical parameters in gastric cancer.
    [Show full text]
  • Defining Natural Antibodies
    PERSPECTIVE published: 26 July 2017 doi: 10.3389/fimmu.2017.00872 Defining Natural Antibodies Nichol E. Holodick1*, Nely Rodríguez-Zhurbenko2 and Ana María Hernández2* 1 Department of Biomedical Sciences, Center for Immunobiology, Western Michigan University Homer Stryker M.D. School of Medicine, Kalamazoo, MI, United States, 2 Natural Antibodies Group, Tumor Immunology Division, Center of Molecular Immunology, Havana, Cuba The traditional definition of natural antibodies (NAbs) states that these antibodies are present prior to the body encountering cognate antigen, providing a first line of defense against infection thereby, allowing time for a specific antibody response to be mounted. The literature has a seemingly common definition of NAbs; however, as our knowledge of antibodies and B cells is refined, re-evaluation of the common definition of NAbs may be required. Defining NAbs becomes important as the function of NAb production is used to define B cell subsets (1) and as these important molecules are shown to play numerous roles in the immune system (Figure 1). Herein, we aim to briefly summarize our current knowledge of NAbs in the context of initiating a discussion within the field of how such an important and multifaceted group of molecules should be defined. Edited by: Keywords: natural antibody, antibodies, natural antibody repertoire, B-1 cells, B cell subsets, B cells Harry W. Schroeder, University of Alabama at Birmingham, United States NATURAL ANTIBODY (NAb) PRODUCING CELLS Reviewed by: Andre M. Vale, Both murine and human NAbs have been discussed in detail since the late 1960s (2, 3); however, Federal University of Rio cells producing NAbs were not identified until 1983 in the murine system (4, 5).
    [Show full text]
  • Flow Reagents Single Color Antibodies CD Chart
    CD CHART CD N° Alternative Name CD N° Alternative Name CD N° Alternative Name Beckman Coulter Clone Beckman Coulter Clone Beckman Coulter Clone T Cells B Cells Granulocytes NK Cells Macrophages/Monocytes Platelets Erythrocytes Stem Cells Dendritic Cells Endothelial Cells Epithelial Cells T Cells B Cells Granulocytes NK Cells Macrophages/Monocytes Platelets Erythrocytes Stem Cells Dendritic Cells Endothelial Cells Epithelial Cells T Cells B Cells Granulocytes NK Cells Macrophages/Monocytes Platelets Erythrocytes Stem Cells Dendritic Cells Endothelial Cells Epithelial Cells CD1a T6, R4, HTA1 Act p n n p n n S l CD99 MIC2 gene product, E2 p p p CD223 LAG-3 (Lymphocyte activation gene 3) Act n Act p n CD1b R1 Act p n n p n n S CD99R restricted CD99 p p CD224 GGT (γ-glutamyl transferase) p p p p p p CD1c R7, M241 Act S n n p n n S l CD100 SEMA4D (semaphorin 4D) p Low p p p n n CD225 Leu13, interferon induced transmembrane protein 1 (IFITM1). p p p p p CD1d R3 Act S n n Low n n S Intest CD101 V7, P126 Act n p n p n n p CD226 DNAM-1, PTA-1 Act n Act Act Act n p n CD1e R2 n n n n S CD102 ICAM-2 (intercellular adhesion molecule-2) p p n p Folli p CD227 MUC1, mucin 1, episialin, PUM, PEM, EMA, DF3, H23 Act p CD2 T11; Tp50; sheep red blood cell (SRBC) receptor; LFA-2 p S n p n n l CD103 HML-1 (human mucosal lymphocytes antigen 1), integrin aE chain S n n n n n n n l CD228 Melanotransferrin (MT), p97 p p CD3 T3, CD3 complex p n n n n n n n n n l CD104 integrin b4 chain; TSP-1180 n n n n n n n p p CD229 Ly9, T-lymphocyte surface antigen p p n p n
    [Show full text]
  • The Impact of the Prostaglandin D2 Receptor 2 and Its Downstream Effects on the Pathophysiology of Asthma
    CORE Metadata, citation and similar papers at core.ac.uk Provided by Ghent University Academic Bibliography Received: 1 March 2019 | Revised: 24 June 2019 | Accepted: 17 July 2019 DOI: 10.1111/all.14001 REVIEW ARTICLE The impact of the prostaglandin D2 receptor 2 and its downstream effects on the pathophysiology of asthma Christopher E. Brightling1 | Guy Brusselle2 | Pablo Altman3 1Department of Respiratory Sciences, Institute for Lung Health, University of Abstract Leicester, Leicester, UK Current research suggests that the prostaglandin D2 (PGD2) receptor 2 (DP2) is a 2 Department of Respiratory Diseases, Ghent principal regulator in the pathophysiology of asthma, because it stimulates and ampli‐ University Hospital, Ghent, Belgium 3Novartis Pharmaceuticals Corporation, East fies the inflammatory response in this condition. The DP2 receptor can be activated Hanover, NJ, USA by both allergic and nonallergic stimuli, leading to several pro‐inflammatory events, Correspondence including eosinophil activation and migration, release of the type 2 cytokines inter‐ Pablo Altman, Novartis Pharmaceuticals leukin (IL)‐4, IL‐5 and IL‐13 from T helper 2 (Th2) cells and innate lymphoid cells type Corporation, One Health Plaza East Hanover, East Hanover, NJ 07936‐1080, 2 (ILCs), and increased airway smooth muscle mass via recruitment of mesenchy‐ USA. mal progenitors to the airway smooth muscle bundle. Activation of the DP2 recep‐ Email: [email protected] tor pathway has potential downstream effects on asthma pathophysiology, including Funding information on airway epithelial cells, mucus hypersecretion, and airway remodelling, and con‐ Novartis sequently might impact asthma symptoms and exacerbations. Given the broad dis‐ tribution of DP2 receptors on immune and structural cells involved in asthma, this receptor is being explored as a novel therapeutic target.
    [Show full text]
  • CXCR6 Within T-Helper (Th) and T-Cytotoxic
    European Journal of Endocrinology (2005) 152 635–643 ISSN 0804-4643 EXPERIMENTAL STUDY CXCR6 within T-helper (Th) and T-cytotoxic (Tc) type 1 lymphocytes in Graves’ disease (GD) G Aust, M Kamprad1, P Lamesch2 and E Schmu¨cking Institute of Anatomy, 1Department of Clinical Immunology and Transfusion Medicine and 2Department of Surgery, University of Leipzig, Phillipp-Rosenthal-Str. 55, Leipzig, 04103, Germany (Correspondence should be addressed to G Aust; Email: [email protected]) Abstract Objective: In Graves’ disease (GD), stimulating anti-TSH receptor antibodies are responsible for hyperthyroidism. T-helper 2 (Th2) cells were expected to be involved in the underlying immune mech- anism, although this is still controversial. The aim of this study was to examine the expression of CXCR6, a chemokine receptor that marks functionally specialized T-cells within the Th1 and T-cyto- toxic 1 (Tc1) cell pool, to gain new insights into the running immune processes. Methods: CXCR6 expression was examined on peripheral blood lymphocytes (PBLs) and thyroid- derived lymphocytes (TLs) of GD patients in flow cytometry. CXCR6 cDNA was quantified in thyroid tissues affected by GD (n ¼ 16), Hashimoto’s thyroiditis (HT; n ¼ 2) and thyroid autonomy (TA; n ¼ 11) using real-time reverse transcriptase PCR. Results: The percentages of peripheral CXCR6þ PBLs did not differ between GD and normal subjects. CXCR6 was expressed by small subsets of circulating T-cells and natural killer (NK) cells. CXCR6þ cells were enriched in thyroid-derived T-cells compared with peripheral CD4þ and CD8þ T-cells in GD. The increase was evident within the Th1 (CD4þ interferon-gþ (IFN-gþ)) and Tc1 (CD8þIFN- gþ) subpopulation and CD8þ granzyme Aþ T-cells (cytotoxic effector type).
    [Show full text]
  • Human Th17 Cells Share Major Trafficking Receptors with Both Polarized Effector T Cells and FOXP3+ Regulatory T Cells
    Human Th17 Cells Share Major Trafficking Receptors with Both Polarized Effector T Cells and FOXP3+ Regulatory T Cells This information is current as Hyung W. Lim, Jeeho Lee, Peter Hillsamer and Chang H. of September 28, 2021. Kim J Immunol 2008; 180:122-129; ; doi: 10.4049/jimmunol.180.1.122 http://www.jimmunol.org/content/180/1/122 Downloaded from References This article cites 44 articles, 15 of which you can access for free at: http://www.jimmunol.org/content/180/1/122.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 28, 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 © 2008 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Human Th17 Cells Share Major Trafficking Receptors with Both Polarized Effector T Cells and FOXP3؉ Regulatory T Cells1 Hyung W. Lim,* Jeeho Lee,* Peter Hillsamer,† and Chang H. Kim2* It is a question of interest whether Th17 cells express trafficking receptors unique to this Th cell lineage and migrate specifically to certain tissue sites.
    [Show full text]