Understanding the Immune System: How It Works
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Lactoferrin and Its Detection Methods: a Review
nutrients Review Lactoferrin and Its Detection Methods: A Review Yingqi Zhang, Chao Lu and Jin Zhang * Department of Chemical and Biochemical Engineering, University of Western Ontario, London, ON N6A 5B9, Canada; [email protected] (Y.Z.); [email protected] (C.L.) * Correspondence: [email protected] Abstract: Lactoferrin (LF) is one of the major functional proteins in maintaining human health due to its antioxidant, antibacterial, antiviral, and anti-inflammatory activities. Abnormal levels of LF in the human body are related to some serious diseases, such as inflammatory bowel disease, Alzheimer’s disease and dry eye disease. Recent studies indicate that LF can be used as a biomarker for diagnosis of these diseases. Many methods have been developed to detect the level of LF. In this review, the biofunctions of LF and its potential to work as a biomarker are introduced. In addition, the current methods of detecting lactoferrin have been presented and discussed. We hope that this review will inspire efforts in the development of new sensing systems for LF detection. Keywords: lactoferrin; biomarkers; immunoassay; instrumental analysis; sensor 1. Introduction Lactoferrin (known as lactotransferrin, LF), with a molecular weight of about 80 kDa, is a functional glycoprotein, which contains about 690 amino acid residues. It was first isolated from bovine milk by Sorensen in 1939 and was first isolated from human milk by Citation: Zhang, Y.; Lu, C.; Zhang, J. Johanson in 1960 [1,2]. The three-dimensional structure of LF has been unveiled by high Lactoferrin and Its Detection resolution X-ray crystallographic analysis, and it consists of two homologous globular lobes Methods: A Review. -
IFM Innate Immunity Infographic
UNDERSTANDING INNATE IMMUNITY INTRODUCTION The immune system is comprised of two arms that work together to protect the body – the innate and adaptive immune systems. INNATE ADAPTIVE γδ T Cell Dendritic B Cell Cell Macrophage Antibodies Natural Killer Lymphocites Neutrophil T Cell CD4+ CD8+ T Cell T Cell TIME 6 hours 12 hours 1 week INNATE IMMUNITY ADAPTIVE IMMUNITY Innate immunity is the body’s first The adaptive, or acquired, immune line of immunological response system is activated when the innate and reacts quickly to anything that immune system is not able to fully should not be present. address a threat, but responses are slow, taking up to a week to fully respond. Pathogen evades the innate Dendritic immune system T Cell Cell Through antigen Pathogen presentation, the dendritic cell informs T cells of the pathogen, which informs Macrophage B cells B Cell B cells create antibodies against the pathogen Macrophages engulf and destroy Antibodies label invading pathogens pathogens for destruction Scientists estimate innate immunity comprises approximately: The adaptive immune system develops of the immune memory of pathogen exposures, so that 80% system B and T cells can respond quickly to eliminate repeat invaders. IMMUNE SYSTEM AND DISEASE If the immune system consistently under-responds or over-responds, serious diseases can result. CANCER INFLAMMATION Innate system is TOO ACTIVE Innate system NOT ACTIVE ENOUGH Cancers grow and spread when tumor Certain diseases trigger the innate cells evade detection by the immune immune system to unnecessarily system. The innate immune system is respond and cause excessive inflammation. responsible for detecting cancer cells and This type of chronic inflammation is signaling to the adaptive immune system associated with autoimmune and for the destruction of the cancer cells. -
White Blood Cells and Severe COVID-19: a Mendelian Randomization Study
Journal of Personalized Medicine Article White Blood Cells and Severe COVID-19: A Mendelian Randomization Study Yitang Sun 1 , Jingqi Zhou 1,2 and Kaixiong Ye 1,3,* 1 Department of Genetics, Franklin College of Arts and Sciences, University of Georgia, Athens, GA 30602, USA; [email protected] (Y.S.); [email protected] (J.Z.) 2 School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China 3 Institute of Bioinformatics, University of Georgia, Athens, GA 30602, USA * Correspondence: [email protected]; Tel.: +1-706-542-5898; Fax: +1-706-542-3910 Abstract: Increasing evidence shows that white blood cells are associated with the risk of coronavirus disease 2019 (COVID-19), but the direction and causality of this association are not clear. To evaluate the causal associations between various white blood cell traits and the COVID-19 susceptibility and severity, we conducted two-sample bidirectional Mendelian Randomization (MR) analyses with summary statistics from the largest and most recent genome-wide association studies. Our MR results indicated causal protective effects of higher basophil count, basophil percentage of white blood cells, and myeloid white blood cell count on severe COVID-19, with odds ratios (OR) per standard deviation increment of 0.75 (95% CI: 0.60–0.95), 0.70 (95% CI: 0.54–0.92), and 0.85 (95% CI: 0.73–0.98), respectively. Neither COVID-19 severity nor susceptibility was associated with white blood cell traits in our reverse MR results. Genetically predicted high basophil count, basophil percentage of white blood cells, and myeloid white blood cell count are associated with a lower risk of developing severe COVID-19. -
Primer the Complement System
View metadata, citation and similar papers at core.ac.uk brought to you by CORE providedMagazine by ElsevierR259 - Publisher Connector vascular permeability and the infection. The second category Primer extravasation of plasma. This is in which there is persistent accompanied by the adhesion of formation of immune complexes is leukocytes to vascular endothelium autoimmune disease, in which, by The complement and their emigration into definition, the antigen is a system surrounding tissue. Complement permanent feature of the host. plays an important part in An understanding of how immune Philip Taylor, Marina inflammation, in helping to recruit complexes cause tissue injury effector cells and in promoting the developed from study of such Botto and Mark Walport killing and clearance of pathogens. diseases in humans and animals, and But complement can be both from the induction of experimental The system of plasma proteins called friend and foe. In some immune complex disease. In these complement was so-named because circumstances the activation of situations, immune complexes were it complements the activity of complement in response to immune shown to cause tissue injury through antibody in the lysis of bacteria. It complexes may cause harm: acutely activation of complement, as opsonin has a central role in host defence in the context of massive (binding to complement receptors on against many micro-organisms and in complement activation occurring in leukocytes) and as the source of the modulation of inflammatory patients with overwhelming Gram- anaphylatoxins (stimulating leukocyte reactions, an activity that has been negative bacterial sepsis, and chemotaxis and degranulation). But illuminated by the study of humans chronically, when an antibody the development of gene-targeted with naturally occurring deficiencies response develops in the context of mice with deficiencies of complement of complement. -
Antibody-Dependent Cellular Cytotoxicity Riiia and Mediate Γ
Effector Memory αβ T Lymphocytes Can Express Fc γRIIIa and Mediate Antibody-Dependent Cellular Cytotoxicity This information is current as Béatrice Clémenceau, Régine Vivien, Mathilde Berthomé, of September 27, 2021. Nelly Robillard, Richard Garand, Géraldine Gallot, Solène Vollant and Henri Vié J Immunol 2008; 180:5327-5334; ; doi: 10.4049/jimmunol.180.8.5327 http://www.jimmunol.org/content/180/8/5327 Downloaded from References This article cites 43 articles, 21 of which you can access for free at: http://www.jimmunol.org/content/180/8/5327.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 © 2008 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Effector Memory ␣ T Lymphocytes Can Express Fc␥RIIIa and Mediate Antibody-Dependent Cellular Cytotoxicity1 Be´atrice Cle´menceau,*† Re´gine Vivien,*† Mathilde Berthome´,*† Nelly Robillard,‡ Richard Garand,‡ Ge´raldine Gallot,*† Sole`ne Vollant,*† and Henri Vie´2*† Human memory T cells are comprised of distinct populations with different homing potential and effector functions: central memory T cells that mount recall responses to Ags in secondary lymphoid organs, and effector memory T cells that confer immediate protection in peripheral tissues. -
Adoptive Cell Therapy Using Engineered Natural Killer Cells
Bone Marrow Transplantation (2019) 54:785–788 https://doi.org/10.1038/s41409-019-0601-6 REVIEW ARTICLE Adoptive cell therapy using engineered natural killer cells Katayoun Rezvani1 © The Author(s), under exclusive licence to Springer Nature Limited 2019 Abstract The generation of autologous T cells expressing a chimeric antigen receptor (CAR) have revolutionized the field of adoptive cellular therapy. CAR-T cells directed against CD19 have resulted in remarkable clinical responses in patients affected by B-lymphoid malignancies. However, the production of allogeneic CAR-T cells products remains expensive and clinically challenging. Moreover, the toxicity profile of CAR T-cells means that currently these life-saving treatments are only delivered in specialized centers. Therefore, efforts are underway to develop reliable off-the-shelf cellular products with acceptable safety profiles for the treatment of patients with cancer. Natural killer (NK) cells are innate effector lymphocytes with potent antitumor activity. The availability of NK cells from multiple sources and their proven safety profile in the allogeneic setting positions them as attractive contenders for cancer immunotherapy. In this review, we discuss advantages and potential drawbacks of using NK cells as a novel cellular therapy against hematologic malignancies, as well as strategies 1234567890();,: 1234567890();,: to further enhance their effector function. Introduction need for inpatient care may ultimately be economically unviable for many health care systems; (iii) the longer time Adoptive cell therapy has become a powerful treatment that is required to generate CAR T-cells may result in modality for advanced cancers refractory to conventional unavoidable delays in therapy, especially for patients with therapy. -
Pathway in the Thymus by a CD24-Dependent Autoreactive T
Autoreactive T Cells Escape Clonal Deletion in the Thymus by a CD24-Dependent Pathway This information is current as Joseph W. Carl, Jr., Jin-Qing Liu, Pramod S. Joshi, Hani Y. of September 27, 2021. El-Omrani, Lijie Yin, Xincheng Zheng, Caroline C. Whitacre, Yang Liu and Xue-Feng Bai J Immunol 2008; 181:320-328; ; doi: 10.4049/jimmunol.181.1.320 http://www.jimmunol.org/content/181/1/320 Downloaded from References This article cites 54 articles, 18 of which you can access for free at: http://www.jimmunol.org/content/181/1/320.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 © 2008 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Autoreactive T Cells Escape Clonal Deletion in the Thymus by a CD24-Dependent Pathway1 Joseph W. Carl, Jr.,* Jin-Qing Liu,* Pramod S. -
Monoclonal Antibody Playbook
Federal Response to COVID-19: Monoclonal Antibody Clinical Implementation Guide Outpatient administration guide for healthcare providers 2 SEPTEMBER 2021 1 Introduction to COVID-19 Monoclonal Antibody Therapy 2 Overview of Emergency Use Authorizations 3 Site and Patient Logistics Site preparation Patient pathways to monoclonal administration 4 Team Roles and Responsibilities Leadership Administrative Clinical Table of 5 Monoclonal Antibody Indications and Administration Indications Contents Preparation Administration Response to adverse events 6 Supplies and Resources Infrastructure Administrative Patient Intake Administration 7 Examples: Sites of Administration and Staffing Patterns 8 Additional Resources 1 1. Introduction to Monoclonal Therapy 2 As of 08/13/21 Summary of COVID-19 Therapeutics 1 • No Illness . Health, no infections • Exposed Asymptomatic Infected . Scope of this Implementation Guide . Not hospitalized, no limitations . Monoclonal Antibodies for post-exposure prophylaxis (Casirivimab + Imdevimab (RGN)) – EUA Issued. • Early Symptomatic . Scope of this Implementation Guide . Not hospitalized, with limitations . Monoclonal Antibodies for treatment (EUA issued): Bamlanivimab + Etesevimab1 (Lilly) Casirivimab + Imdevimab (RGN) Sotrovimab (GSK/Vir) • Hospital Adminission. Treated with Remdesivir (FDA Approved) or Tocilizumab (EUA Issued) . Hospitalized, no acute medical problems . Hospitalized, not on oxygen . Hospitlaized, on oxygen • ICU Admission . Hospitalized, high flow oxygen, non-invasive ventilation -
Natural Killer T Cells Are Required for the Development of a Superantigen-Driven T Helper Type 2 Immune Response in Mice
IMMUNOLOGY ORIGINAL ARTICLE Natural killer T cells are required for the development of a superantigen-driven T helper type 2 immune response in mice Auro Nomizo,1 Edilberto Postol,2 Summary Raquel de Alencar,2 Fabı´ola We show, here, that one single injection or weekly injections of staphylo- Cardillo2 and Jose´ Mengel2 coccal enterotoxin B (SEB), starting in 1-day-old newborn mice, induced 1Department of Clinical Analysis, Toxicology a powerful immune response with a T helper type 2 (Th2) pattern, as and Bromatology, Faculty of Pharmaceutical Sciences of Ribeira˜o Preto, University of Sa˜o judged by the isotype and cytokine profile, with the production of large Paulo, Ribeira˜o Preto, and 2Department of amounts of SEB-specific immunoglobulin G1 (IgG1), detectable levels of Immunology, Institute of Biomedical Sciences, SEB-specific IgE and increased production of interleukin-4 by spleen cells. University of Sa˜o Paulo, Sa˜o Paulo, SP, Brazil These protocols also induced an increase in the levels of total IgE in the serum. Memory of SEB was transferred to secondary recipients by using total spleen cells from primed animals. The secondary humoral response in transferred mice was diminished if spleen cells from SEB-treated mice were previously depleted of CD3+ or Vb8+ T cells or NK1.1+ cells. In vivo depletion of NK1.1+ cells in adult mice resulted in a marked reduction in the SEB-specific antibody response in both the primary and secondary doi:10.1111/j.1365-2567.2005.02215.x immune responses. Additionally, purified NK1.1+ T cells were able to per- Received 11 April 2005; revised 23 May 2005; form SEB-specific helper B-cell actions in vitro and in vivo. -
Apheresis Donation This Quick Reference Guide Will Help You Identify the Best Donation for Your Unique Blood Type
Apheresis Donation This quick reference guide will help you identify the best donation for your unique blood type. Donors now have the opportunity to make an apheresis (ay-fur-ee-sis) donation and donate just platelets, red cells, or plasma at blood drives. These individual components are vital for local patients in need. Platelets Control Bleeding Red Cells Deliver Oxygen Plasma transports blood cells & controls bleeding Donation Type Blood Types Requirements Donation Time A+, B+, O+ Over 75% of population has one of these blood types. Platelet Donation: Be healthy, weigh at least 114 lbs 2 hours cancer & surgery patients no aspirin for 48 hours Platelets only last five days after donation so the need is constant. O-, O+, A-, B- Special height, weight, Double Red: O-Negative is the 1 hour and hematocrit requirements. surgery, trauma patients, universal red cell donor. +25 min Please call us or see a staff member accident, & burn victims Only 17% of population has one of these negative blood types Plasma: AB+, AB- Trauma patients, burn Universal Plasma Donors 1 hour Be healthy, weigh at least 114 lbs victims, & patients with +30 min serious illness or injuries Only 4% of population How Apheresis works: Blood is drawn from the donor’s arm and the components are separated. Only the components being donated are collected while the remaining components are safely returned to the donor How to Schedule an Appointment: Please call 800-398-7888 or visit schedule.bloodworksnw.org. Walk-ins are also welcome at some blood drives, so be sure to ask our staff when you stop in. -
Foundation Block Lecture Three Cell Mediated Immunity
Foundation Block Lecture Five Hypersensitivity Objectives: • To know that hypersensitivity reactions are over and excessive immune responses that can be harmful to body in four different ways • To be familiar with inflammatory processes in type I hypersensitivity reaction that mediates allergic inflammation • To recognize that type II hypersensitivity deals with immune responses against antigens that are integral part of cell membrane and are usually associated with autoimmune disorders • To know that type III hypersensitivity reactions are mediated by immune complexes and cause vasculitis • To describe type IV hypersensitivity is a purely cell mediated immune response associated with chronic inflammation ● Important. ● Extra notes. ● Females notes ● Males notes. What is hypersensitivity? Protective immunity: desirable reaction. Hypersensitivity: undesirable damaging reaction produced by excessive immune reactions. - Undesirable responses can be mediated by: - Antibody binding to antigens (Types I-III). - Cell mediated reaction to chemicals or proteins (Type IV). Types of hypersensitivity: 4 Types of hypersensitivity responses are classified by GEL AND COOMBS (names of scientists) according to the responding mechanisms, NOT the responding antigens: *From 433 team Type I: 1- Also termed as: - Immediate Hypersensitivity. - Allergic reactions. (e.g. asthma and eczema) - Anaphylactic reactions: severe and rapidly progressing systemic forms which can be quickly life threatening. …..............(causes.vasodilation and hypovolemia which causes heart stop then death) 2- Most people will not react to these allergens but some individuals “atopic” respond by producing large amounts of IgE in …........response to those otherwise harmless substances. 3- Non-allergic individuals respond to these allergens by producing IgG antibodies. 4- Features: - Antibody type: IgE - Cellular components: Mast cells, basophiles & eosinophils - Antigens: Also known as allergens ( antigens with low molecular weight & highly soluble). -
B Cell Checkpoints in Autoimmune Rheumatic Diseases
REVIEWS B cell checkpoints in autoimmune rheumatic diseases Samuel J. S. Rubin1,2,3, Michelle S. Bloom1,2,3 and William H. Robinson1,2,3* Abstract | B cells have important functions in the pathogenesis of autoimmune diseases, including autoimmune rheumatic diseases. In addition to producing autoantibodies, B cells contribute to autoimmunity by serving as professional antigen- presenting cells (APCs), producing cytokines, and through additional mechanisms. B cell activation and effector functions are regulated by immune checkpoints, including both activating and inhibitory checkpoint receptors that contribute to the regulation of B cell tolerance, activation, antigen presentation, T cell help, class switching, antibody production and cytokine production. The various activating checkpoint receptors include B cell activating receptors that engage with cognate receptors on T cells or other cells, as well as Toll-like receptors that can provide dual stimulation to B cells via co- engagement with the B cell receptor. Furthermore, various inhibitory checkpoint receptors, including B cell inhibitory receptors, have important functions in regulating B cell development, activation and effector functions. Therapeutically targeting B cell checkpoints represents a promising strategy for the treatment of a variety of autoimmune rheumatic diseases. Antibody- dependent B cells are multifunctional lymphocytes that contribute that serve as precursors to and thereby give rise to acti- cell- mediated cytotoxicity to the pathogenesis of autoimmune diseases