DOCSLIB.ORG

B Cell Responses: Plasmablasts Walk the Line

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
B Cell Responses: Plasmablasts Walk the Line RESEARCH HIGHLIGHTS B CELL RESPONSES Plasmablasts walk the line During an adaptive immune patterns in lymph nodes. Following molecule intercellular adhesion response, long-lived antibody- immunization with specific antigen, molecule 1 (ICAM1) in plasmablast producing plasma cells are generated YFP+ cells mainly aggregated in migration. Both YFP+ and naive in T cell-dependent germinal centres. the medulla of the lymph node but B cells migrated on ICAM1-coated Plasma cells subsequently localize to could also be found in the B and glass surfaces, but only naive B cells the lymph node medullary chords, T cell zones and at the border of required Gαi-signalling for this move- but their migration to these sites has germinal centres. By contrast, naive ment. In addition, naive B cells and never been directly observed. A study B cells were predominantly localized plasma blasts had different migratory in Immunity has now reported in B cell follicles. behaviour on the ICAM1-coated sur- unique migratory behaviour for their When the migratory patterns faces; naive B cells showed frequent precursors, plasmablasts; these cells of the different populations were detachment and reattachment to the traverse the lymph node in a linear observed in situ using time-lapse substrate, but YFP+ cells migrated in manner and, surprisingly, do not two-photon intravital microscopy, a steady, amoeboid manner. + require Gαi-coupled receptor YFP cells in the medullary chords Interestingly, in assays carried signalling to migrate. were found to be mainly stationary, out in vivo and in vitro, the authors The transcriptional repressor but YFP+ cells in the follicles were reported an inverse correlation B lymphocyte-induced maturation highly motile. Naive B cells showed between cell speed and cellular YFP protein 1 (BLIMP1) is crucial for random, winding patterns of motion, intensity as BLIMP1 expression plasma cell differentiation and is an but migration of extramedullary increases during plasma cell matura- early marker of plasma cell devel- YFP+ cells was steady and linear. tion; this suggests that plasmablast opment. BLIMP1–yellow fluores- Despite having decreased migratory migration and arrest is cell auto- cent protein (BLIMP1YFP) reporter speeds compared with naive B cells, nomous. Finally, although plasma- mice expressing a transgenic B cell YFP+ cells had higher rates of dis- blasts could migrate independently receptor were therefore used to placement, consistent with these cells of Gαi-mediated signalling, PTX visualize plasma cell migration moving in a constant, linear manner. treatment at early time points follow- However, YFP+ cells did not show any ing immunization decreased plasma evidence of directional movement, cell accumulation in the medulla; suggesting that plasmablasts do not however, YFPhi cells were enriched use preformed chemotactic gradients in the B and T cell zones following to travel to the medulla. PTX treatment, suggesting that To more closely examine the plasmablast maturation is also cell role of chemokines in plasmablast autonomous. migration, the authors treated cells The authors propose a model in with pertussis toxin (PTX), which which plasmablasts seek out medul- blocks Gαi-mediated signalling and lary cords by undertaking random, prevents most chemokine-directed linear migration paths. Both the movement. Strikingly, whereas PTX migration and maturation of plasma- treatment inhibited naive B cell blasts seem to be cell autonomous, migration, PTX-treated YFP+ cells but chemokine receptor signalling continued to crawl in a persistent, may be required for plasma cell linear manner. Further experiments retention in the medulla. using the inhibitor FTY720 indicated Yvonne Bordon This image is taken from a time-lapse movie, which visualized a mouse popliteal lymph that plasmablast migration in the node during an immune response by two-photon intravital microscopy. A newly lymph node was also independent ORIGINAL RESEARCH PAPER Fooksman, D. R. generated plasmablast (green) is emigrating from a germinal centre (red), with naive of sphingosine-1-phosphate (S1P) et al. Development and migration of plasma cells B cells (blue) in the follicle. The cell track (grey) shows a highly linear path over a period of receptor signalling. The authors next in the mouse lymph node. Immunity 8 Jul 2010 75 minutes. Image courtesy of D. R. Fooksman, New York University School of Medicine, (doi:10.1016/j.immuni.2010.06.015) New York, USA. 2010 Elsevier. assessed the role of the adhesion NATURE REVIEWS | IMMUNOLOGY VOLUME 10 | AUGUST 2010 © 2010 Macmillan Publishers Limited. All rights reserved.
Load more

Recommended publications
  • B Cell Activation and Escape of Tolerance Checkpoints: Recent Insights from Studying Autoreactive B Cells
    cells Review B Cell Activation and Escape of Tolerance Checkpoints: Recent Insights from Studying Autoreactive B Cells Carlo G. Bonasia 1 , Wayel H. Abdulahad 1,2 , Abraham Rutgers 1, Peter Heeringa 2 and Nicolaas A. Bos 1,* 1 Department of Rheumatology and Clinical Immunology, University Medical Center Groningen, University of Groningen, 9713 Groningen, GZ, The Netherlands; [email protected] (C.G.B.); [email protected] (W.H.A.); [email protected] (A.R.) 2 Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, 9713 Groningen, GZ, The Netherlands; [email protected] * Correspondence: [email protected] Abstract: Autoreactive B cells are key drivers of pathogenic processes in autoimmune diseases by the production of autoantibodies, secretion of cytokines, and presentation of autoantigens to T cells. However, the mechanisms that underlie the development of autoreactive B cells are not well understood. Here, we review recent studies leveraging novel techniques to identify and characterize (auto)antigen-specific B cells. The insights gained from such studies pertaining to the mechanisms involved in the escape of tolerance checkpoints and the activation of autoreactive B cells are discussed. Citation: Bonasia, C.G.; Abdulahad, W.H.; Rutgers, A.; Heeringa, P.; Bos, In addition, we briefly highlight potential therapeutic strategies to target and eliminate autoreactive N.A. B Cell Activation and Escape of B cells in autoimmune diseases. Tolerance Checkpoints: Recent Insights from Studying Autoreactive Keywords: autoimmune diseases; B cells; autoreactive B cells; tolerance B Cells. Cells 2021, 10, 1190. https:// doi.org/10.3390/cells10051190 Academic Editor: Juan Pablo de 1.
    [Show full text]
  • Overview of B-Cell Maturation, Activation, Differentiation
    Overview of B-Cell Maturation, Activation, Differentiation B-Cell Development Begins in the Bone Marrow and Is Completed in the Periphery Antigen-Independent (Maturation) 1) Pro-B stages B-cell markers 2) Pre B-stages H- an L- chain loci rearrangements surrogate light chain 3) Naïve B-cell functional BCR . B cells are generated in the bone marrow. Takes 1-2 weeks to develop from hematopoietic stem (HSC) cells to mature B cells. Sequence of expression of cell surface receptor and adhesion molecules which allows for differentiation of B cells, proliferation at various stages, and movement within the bone marrow microenvironment. HSC passes through progressively more delimited progenitor-cell stages until it reaches the pro-B cell stage. Pre-B cell is irreversibly committed to the B-cell lineage and the recombination of the immunoglobulin genes expressed on the cell surface Immature B cell (transitional B cell) leaves the bone marrow to complete its maturation in the spleen through further differentiation. Immune system must create a repertoire of receptors capable of recognizing a large array of antigens while at the Source: Internet same time eliminating self-reactive B cells. B-Cell Activation and Differentiation • Exposure to antigen or various polyclonal mitogens activates resting B cells and stimulates their proliferation. • Activated B cells lose expression of sIgD and CD21 and acquire expression of activation antigens. Growth factor receptors, structures involved in cell-cell interaction, molecules that play a role in the localization and binding of activated B cells Two major types: T cell dependent (TD) T cell independent (TI) B-Cell Activation by Thymus-Independent and Dependent Antigens Source: Kuby T cell dependent: Involves protein antigens and CD4+ helper T cells.
    [Show full text]
  • Our Immune System (Children's Book)
    OurOur ImmuneImmune SystemSystem A story for children with primary immunodeficiency diseases Written by IMMUNE DEFICIENCY Sara LeBien FOUNDATION A note from the author The purpose of this book is to help young children who are immune deficient to better understand their immune system. What is a “B-cell,” a “T-cell,” an “immunoglobulin” or “IgG”? They hear doctors use these words, but what do they mean? With cheerful illustrations, Our Immune System explains how a normal immune system works and what treatments may be necessary when the system is deficient. In this second edition, a description of a new treatment has been included. I hope this book will enable these children and their families to explore together the immune system, and that it will help alleviate any confusion or fears they may have. Sara LeBien This book contains general medical information which cannot be applied safely to any individual case. Medical knowledge and practice can change rapidly. Therefore, this book should not be used as a substitute for professional medical advice. SECOND EDITION COPYRIGHT 1990, 2007 IMMUNE DEFICIENCY FOUNDATION Copyright 2007 by Immune Deficiency Foundation, USA. Readers may redistribute this article to other individuals for non-commercial use, provided that the text, html codes, and this notice remain intact and unaltered in any way. Our Immune System may not be resold, reprinted or redistributed for compensation of any kind without prior written permission from Immune Deficiency Foundation. If you have any questions about permission, please contact: Immune Deficiency Foundation, 40 West Chesapeake Avenue, Suite 308, Towson, MD 21204, USA; or by telephone at 1-800-296-4433.
    [Show full text]
  • B-Cell Reconstitution Recapitulates B-Cell Lymphopoiesis Following Haploidentical BM Transplantation and Post-Transplant CY
    Bone Marrow Transplantation (2015) 50, 317–319 © 2015 Macmillan Publishers Limited All rights reserved 0268-3369/15 www.nature.com/bmt LETTER TO THE EDITOR B-cell reconstitution recapitulates B-cell lymphopoiesis following haploidentical BM transplantation and post-transplant CY Bone Marrow Transplantation (2015) 50, 317–319; doi:10.1038/ From week 9, the proportion of transitional B cells progressively bmt.2014.266; published online 24 November 2014 decreased (not shown), whereas that of mature B cells increased (Figure 1d). To further evaluate the differentiation of mature cells, we included markers of naivety (IgM and IgD) and memory (IgG) in The treatment of many hematological diseases benefits from our polychromatic panel. At week 9, when a sufficient proportion myeloablative or non-myeloablative conditioning regimens of cells were available for the analysis, B cells were mostly naive followed by SCT or BMT. HLA-matched donors are preferred but and remained so for 26 weeks after haploBMT (Figure 1d). Despite not always available. Instead, haploidentical donors can be rapidly low, the proportion of memory B cells reached levels similar to identified. Unmanipulated haploidentical BMT (haploBMT) with that of marrow donors (Supplementary Figure 1D). non-myeloablative conditioning and post-transplant Cy has been To further investigate the steps of B-cell maturation, we developed to provide a universal source of BM donors.1 Cy, analyzed CD5, a regulator of B-cell activation, and CD21, a which depletes proliferating/allogeneic cells, prevents GVHD.1 component of the B-cell coreceptor complex, on transitional B Importantly, the infection-related mortality was remarkably low, cells. These surface markers characterize different stages of 5,6 5,6 suggesting effective immune reconstitution.1,2 However, a transitional B-cell development.
    [Show full text]
  • Human B Cell Isolation Product Selection Diagram
    Human B Cell Isolation Product Selection Explore the infographic below to find the correct human B cell isolation product for your application. 1. Your Starting Sample Whole Peripheral Blood/Buffy Coat PBMCs/Leukapheresis Pack 2. Cell Separation Platform Immunodensity Cell Separation Immunomagnetic Cell Separation Immunomagnetic Cell Separation 3. Product Line RosetteSep™ EasySep™ EasySep™ Sequential Selection Negative Selection Negative Selection Positive Selection Negative Selection Positive Selection 4. Selection Method (Positive + Negative) iRosetteSep™ HLA iEasySep™ Direct HLA i, iiEasySep™ HLA iEasySep™ HLA B Cell viEasySep™ Human CD19 EasySep™ Human IgG+ B Cell Enrichment Cocktail B Cell Isolation Kit Chimerism Whole Blood Enrichment Kit Positive Selection Kit II Memory B Cell Isolation (15064HLA)1, 2, 3 (89684) / EasySep™ Direct B Cell Positive Selection (19054HLA)1, 2 (17854)1, 2 Kit (17868)1 (optional), 2' HLA Crossmatch B Cell Kit (17886)1, 2 Isolation Kit (19684 - 1, 2 RosetteSep™ Human available in the US only) iiiEasySep™ Human B Cell viEasySep™ Release EasySep™ Human Memory 5. Cell Isolation Kits B Cell Enrichment Cocktail i, iiEasySep™ HLA Enrichment Kit Human CD19 Positive B Cell Isolation Kit 1, 2, 3 1, 2 1, 2 1 (optional), 2 Catalog #s shown in ( ) (15024) Chimerism Whole Blood (19054) Selection Kit (17754) (17864) EasySep™ Direct Human CD19 Positive Selection B-CLL Cell Isolation Kit Kit (17874)1, 2 1, 2, 3, 4 *RosetteSep™ Human (19664) iiiEasySep™ Human B Cell EasySep™ Human CD138 Multiple Myeloma Cell Isolation Kit
    [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]
  • Med-Pathway Zoom Workshop
    MCAT Immunology Dr. Phillip Carpenter medpathwaymcat Med-pathway AAMC MCAT Content Outline: Immunology Category 1A: Structure/Function of Proteins/AA Immune System Category 3B: Organ Systems Innate vs. Adaptive Immunity T and B Lymphocytes Macrophages & Phagocytes Tissue-Bone marrow, Spleen, Thymus, Lymph nodes Antigen and Antibody Antigen Presentation Clonal Selection Antigen-Antibody recognition Structure of antibody molecule Self vs. Non-self, Autoimmune Diseases Major Histocompatibility Complex Lab Techniques: ELISA & Western Blotting Hematopoiesis Creates Immune Cells Self vs. Non-self Innate vs Adaptive Innate Immunity Physical Barriers: Skin, mucous membranes, pH Inflammatory mediators: Complement, Cytokines, Prostaglandins Cellular Components: Phagocytes-Neutrophils, Eosinophils, Basophils, Mast Cells Antigen Presenting Cells-Monocytes, Macrophages, Dendritic Cells Adaptive (Acquired) Immunity Composed of B and T lymphocytes: Activated by Innate Immunity B cells: Express B cell receptor and secrete antibodies as plasma cells T cells: Mature in thymus, express TCR surface receptor; Activated by Antigen Presenting Cells (APCs) Direct Immune response (The Ringleaders of immune system) Major Lymphoid Organs TYPE SITE FUNCTION Fetal production of Liver 1° lymphoid cells Hematopoietic production of 1° Bone marrow myeloid and lymphoid cells Receives bone marrow T 1° Thymus cells; site where self is selected from non-self Lymph nodes 2° Sites of antigen activation Spleen of lymphocytes; clearance Macrophages (Sentinel Cells) Pattern Recognition
    [Show full text]
  • 1 the Immune System
    1 The immune system The immune response Innate immunity Adaptive immunity The immune system comprises two arms (rapid response) (slow response) functioning cooperatively to provide a Dendritic cell Mast cell comprehensive protective response: the B cell innate and the adaptive immune system. Macrophage γδ T cell T cell The innate immune system is primitive, does not require the presentation of an antigen, Natural and does not lead to immunological memory. killer cell Basophil Its effector cells are neutrophils, Complement protein macrophages, and mast cells, reacting Antibodies Natural Eosinophil killer T cell CD4+ CD8+ within minutes to hours with the help of T cell T cell complement activation and cytokines (CK). Granulocytes Neutrophil B-lymphocytes B-cell receptor The adaptive immune response is provided by the lymphocytes, which precisely recognise unique antigens (Ag) through cell-surface receptors. epitope Receptors are obtained in billions of variations through antigen cut and splicing of genes and subsequent negative T-lymphocytes selection: self-recognising lymphocytes are eradicated. T-cell receptor Immunological memory after an Ag encounter permits a faster and heightened state of response on a subsequent exposure. epitope MHC Lymphocytes develop in primary lymphoid tissue (bone marrow [BM], thymus) and circulate towards secondary Tonsils and adenoids Lymph lymphoid tissue (lymph nodes [LN], spleen, MALT). nodes Lymphatic vessels The Ag reach the LN carried by lymphocytes or by Thymus dendritic cells. Lymphocytes enter the LN from blood Lymph transiting through specialised endothelial cells. nodes The Ag is processed within the LN by lymphocytes, Spleen macrophages, and other immune cells in order to mount a specific immune response.
    [Show full text]
  • Homeostatic and Activated Conditions Cell
    The Journal of Immunology Dynamics of the Splenic Innate-like CD19+CD45Rlo Cell Population from Adult Mice in Homeostatic and Activated Conditions Bele´n de Andre´s,*,1 Carmen Prado,* Beatriz Palacios,* Mario Alı´a,* Sharmili Jagtap,† Natalia Serrano,† Isabel Cortegano,* Miguel Angel R. Marcos,† and Maria Luisa Gaspar*,1 In the adult spleen, CD19+CD45R2/lo (19+45Rlo) lymphocytes of embryonic origin exist as a distinct population to that of the conventional B cell lineage. These cells display a plasmablast phenotype, and they spontaneously secrete IgG1 and IgA, whereas the bone marrow population of 19+45Rlo cells contains B1 progenitors. In this study, we show that 19+45Rlo cells are also present in Peyer’s patches and in the spleen throughout the life span of wild-type mice, beginning at postnatal day 7. Although this population is heterogeneous, the surface phenotype of most of these cells distinguishes them from follicular, transitional, marginal zone, and B1 cells. In CBA/CaHN mice, few 19+45Rlo cells were detected at postnatal day 7, and none was observed in the adult spleen. Splenic 19+45Rlo cells exhibited homeostatic BrdU uptake in vivo and actively transcribed cell cycle genes. When trans- ferred to immunodeficient RAG22/2gchain2/2 recipient mice, 19+45Rlo cells survived and differentiated into IgG1– and IgA– plasma cells. Moreover, in vitro stimulation of splenic 19+45Rlo cells with LPS, CpG, BAFF/IL4, and CD40/IL4 induced cell proliferation, IgG1/IgA secretion and the release of IL-10, suggesting a potential immunoregulatory role for this subset of innate- like B cells. The Journal of Immunology, 2012, 189: 2300–2308.
    [Show full text]
  • B-Cell Lymphomas Differ in Their Responsiveness to Cpg Oligodeoxynucleotides
    1490 Vol. 11, 1490–1499, February 15, 2005 Clinical Cancer Research B-Cell Lymphomas Differ in their Responsiveness to CpG Oligodeoxynucleotides Bernd Jahrsdorfer,5 Lars Mu¨hlenhoff,1 responsiveness to CpG oligodeoxynucleotides. Focusing Sue E. Blackwell,5 Moritz Wagner,1 clinical studies on patients with highly CpG oligodeoxynu- cleotide–sensitive B-cell malignancies may improve the Hendrik Poeck,1 Evelyn Hartmann,3 Ralf Jox,1 clinical outcome of such trials. Thomas Giese,4 Bertold Emmerich,2 Stefan Endres,1 5 1 George J. Weiner, and Gunther Hartmann INTRODUCTION 1 2 Division of Clinical Pharmacology and Department of Internal The vast majority of lymphoid neoplasms worldwide are Medicine, Division of Hematology, and 3Department of Otorhinolaryngology, University of Munich, Munich, Germany; derived from B lymphocytes at various stages of differentiation. 4Institute of Immunology, University of Heidelberg, Heidelberg, Neoplasms originating from precursor B cells are rare. Neo- Germany; and 5Holden Comprehensive Cancer Center and plasms derived from mature naive B cells include B-cell chronic Department of Internal Medicine, University of Iowa, Iowa City, Iowa lymphocytic leukemia (B-CLL), B-cell small lymphocytic lymphoma (SLL), and mantle cell lymphoma (MCL). Follicular lymphoma (FL) and diffuse large B-cell lymphoma (LCL) are ABSTRACT derived from germinal center B cells. Memory B cells can Human B cells detect CpG motifs within microbial DNA develop into marginal zone B-cell lymphoma (MZL) and B- via TLR9. Synthetic CpG oligodeoxynucleotides are currently CLL. Plasmacytoma is related to plasma cells (1). The most being tested in clinical trials for the therapy of different types typical lymphomas are of diffuse large B-cell type (33%) of B cell non-Hodgkin’s lymphoma.
    [Show full text]
  • Human Naive B Cells Cells by Cpg Oligodeoxynucleotide-Primed T+
    Presentation of Soluble Antigens to CD8+ T Cells by CpG Oligodeoxynucleotide-Primed Human Naive B Cells This information is current as Wei Jiang, Michael M. Lederman, Clifford V. Harding and of September 27, 2021. Scott F. Sieg J Immunol 2011; 186:2080-2086; Prepublished online 14 January 2011; doi: 10.4049/jimmunol.1001869 http://www.jimmunol.org/content/186/4/2080 Downloaded from References This article cites 36 articles, 21 of which you can access for free at: http://www.jimmunol.org/content/186/4/2080.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 27, 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 © 2011 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Presentation of Soluble Antigens to CD8+ T Cells by CpG Oligodeoxynucleotide-Primed Human Naive B Cells Wei Jiang,*,† Michael M. Lederman,*,† Clifford V. Harding,†,‡ and Scott F. Sieg*,† Naive B lymphocytes are generally thought to be poor APCs, and there is limited knowledge of their role in activation of CD8+ T cells.
    [Show full text]
  • Plasma Cells: Finding New Light at the End of B Cell Development Kathryn L
    © 2001 Nature Publishing Group http://immunol.nature.com REVIEW Plasma cells: finding new light at the end of B cell development Kathryn L. Calame Plasma cells are cellular factories devoted entire- Upon plasma cell differentiation, there is a marked increase in ly to the manufacture and export of a single prod- steady-state amounts of Ig heavy and light chain mRNA and, when 2 uct: soluble immunoglobulin (Ig). As the final required for IgM and IgA secretion, J chain mRNA . Whether the increase in Ig mRNA is due to increased transcription, increased mediators of a humoral response, plasma cells mRNA stability or, as seems likely, both mechanisms, remains con- play a critical role in adaptive immunity.Although troversial2. There is also an increase in secreted versus membrane intense effort has been devoted to studying the forms of heavy chain mRNA, as determined by differential use of poly(A) sites that may involve the availability of one component of regulation and requirements for early B cell the polyadenylation machinery, cleavage-stimulation factor Cst-643. development, little information has been avail- To accommodate translation and secretion of the abundant Ig able on plasma cells. However, more recent mRNAs, plasma cells have an increased cytoplasmic to nuclear ratio work—including studies on genetically altered and prominent amounts of rough endoplasmic reticulum and secreto- ry vacuoles. mice and data from microarray analyses—has Numerous B cell–specific surface proteins are down-regulated begun to identify the regulatory cascades that upon plasma cell differentiation, including major histocompatibility initiate and maintain the plasma cell phenotype. complex (MHC) class II, B220, CD19, CD21 and CD22.
    [Show full text]