Psoriasis Review
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Biologic Armamentarium in Psoriasis
Vol 9, Issue 1, 2016 ISSN - 0974-2441 Review Article BIOLOGIC ARMAMENTARIUM IN PSORIASIS GANESH PAI1*, NITHIN SASHIDHARAN2 1Medical Director, Derma-Care ‘The Trade Centre’, Mangalore - 575 003, Karnataka, India. 2Consultant Clinical Pharmacologist, Derma-Care ‘The Trade Centre’, Mangalore - 575 003, Karnataka, India. Email: [email protected] Received: 14 July 2015, Revised and Accepted: 24 August 2015 ABSTRACT Psoriasis is an autoimmune disease and further classed as a chronic inflammatory skin condition serving as a global burden. A moderate to severe psoriasis can be treated with conventional therapies. Less efficacy, poor patient compliance, and toxicity issues were the major problems associated with conventional therapies. The introduction of biologic therapy has a great impression on psoriatic treatment duration and enhanced quality of life in psoriasis patients. The new biologic therapies are tailor-made medications with the goal of more specific and effective treatment; less toxicity. The biologic therapy is aimed to target antigen presentation and co-stimulation, T-cell activation, and leukocyte adhesion; and pro-inflammatory cascade. They act as effective and safer substitute to traditional therapy. Secukinumab, certolizumab, itolizumab, golimumab, ustekinumab, adalimumab, infliximab etanercept, alefacept, etc. are the approved biologic with the global market. This review briefs about psoriasis pathogenesis, traditional treatments, and biologic therapies potential. Keywords: Psoriasis, Biologic, Non-biologic treatment. INTRODUCTION migration, potentiation of Th1 type of response, angiogenesis, and epidermal hyperplasia [7]. Psoriasis is an autoimmune disease and further classed as a chronic inflammatory skin condition with prevalence ranging 1-3% in the TNF- is plays vital role in the pathogenesis of psoriasis. It acts by world [1]. -
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Antibodies to Watch in a Pandemic Dr. Janice M. Reichert, Executive Director, The Antibody Society August 27, 2020 (updated slides) Agenda • US or EU approvals in 2020 • Granted as of late July 2020 • Anticipated by the end of 2020 • Overview of antibody-based COVID-19 interventions in development • Repurposed antibody-based therapeutics that treat symptoms • Newly developed anti-SARS-CoV-2 antibodies • Q&A 2 Number of first approvals for mAbs 10 12 14 16 18 20 Annual first approvals in either the US or EU or US the either in approvals first Annual 0 2 4 6 8 *Estimate based on the number actually approved and those in review as of July 15, with assumption of approval on the first c first the on of approval assumption 15, with as July of review in those and approved actually number the on based *Estimate Tables of approved mAbs and antibodies in review available at at mAbs ofand available in antibodies approved review Tables 1997 98 99 2000 01 02 03 Year of first US or EU approval or EU US of first Year 04 05 06 https://www.antibodysociety.org/resources/approved 07 08 09 10 11 12 13 14 15 Non-cancer Cancer 16 - antibodies/ 17 ycl 18 e. 19 2020* First approvals US or EU in 2020 • Teprotumumab (Tepezza): anti-IGF-1R mAb for thyroid eye disease • FDA approved on January 21 • Eptinezumab (Vyepti): anti-CGRP IgG1 for migraine prevention • FDA approved on February 21 • Isatuximab (Sarclisa): anti-CD38 IgG1 for multiple myeloma • FDA approved on March 2, also approved in the EU on June 2 • Sacituzumab govitecan (Trodelvy): anti-TROP-2 ADC for triple-neg. -
Clinical and Basic Immunodermatology Clinical and Basic Immunodermatology
Clinical and Basic Immunodermatology Clinical and Basic Immunodermatology Edited by Anthony A. Gaspari, MD Department of Dermatology University of Maryland School of Medicine Baltimore, MD USA Stephen K. Tyring, MD, PhD Department of Dermatology University of Texas Medical School at Houston Houston, TX USA Editors Anthony A. Gaspari, MD University of Maryland School of Medicine Baltimore, MD USA Stephen K. Tyring, MD, PhD University of Texas Medical School at Houston Houston, TX USA ISBN 978-1-84800-164-0 e-ISBN 978-1-84800-165-7 DOI 10.1007/978-1-84800-165-7 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Control Number: 2008923739 © Springer-Verlag London Limited 2008 Apart from any fair dealing for the purposes of research or private study, or criticism or review, as permitted under the Copyright, Designs and Patents Act 1988, this publication may only be reproduced, stored or transmitted, in any form or by any means, with the prior permission in writing of the publishers, or in the case of reprographic reproduction in accordance with the terms of licences issued by the Copyright Licensing Agency. Enquiries concerning reproduction outside those terms should be sent to the publishers. The use of registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant laws and regulations and therefore free for general use. Product liability: The publisher can give no guarantee for information about drug dosage and application thereof contained in this book. -
Immunodermatology
Editorial Volume 8:2,2021 Journal of Dermatology and Dermatologic Diseases ISSN: 2684-4281 Open Access Editorial Note on Immunodermatology Bindu Madhavi* Department of Biotechnology, Vignan’s University, Vadlamudi Editorial Immunodermatology studies the skin as an invulnerable organ of both health and infection. Many ranges, such as photographic immunology (impacts of ultraviolet light on skin resistance), provocative diseases, are uncommonly considered, For starters, unfavourably prone contact dermatitis and atopic inflammation of the skin, immune system-related skin conditions such as vitiligo and psoriasis, and finally, the immunology of microbial skin infections such as retrovirus contamination and impurity. This area has some experience treating non-susceptible interceptible skin diseases like lupus, bullous pemphigoid, pemphigus vulgaris, and other skin problems that can be safely intervened. The skin has a great influence on ensuring shape against infection as an unpredictable invulnerable organ. Inalienable resistance requires an early reaction to remote antigens, so it is not a specific pathogen, whereas an adjustable reaction to the differentiation of antigens and the advancement of memory is specific, but it takes more time to function. Infections have strengthened mechanisms to prevent their descendants from contaminating or discharging the skin-resistant reaction. By managing a rapid invulnerable response, with abnormal levels of protective antibodies to their target viral antigens, immunizations may safeguard against infections. -
Clinical and Basic Immunodermatology Clinical and Basic Immunodermatology
Clinical and Basic Immunodermatology Clinical and Basic Immunodermatology Edited by Anthony A. Gaspari, MD Department of Dermatology University of Maryland School of Medicine Baltimore, MD USA Stephen K. Tyring, MD, PhD Department of Dermatology University of Texas Medical School at Houston Houston, TX USA Editors Anthony A. Gaspari, MD University of Maryland School of Medicine Baltimore, MD USA Stephen K. Tyring, MD, PhD University of Texas Medical School at Houston Houston, TX USA ISBN 978-1-84800-164-0 e-ISBN 978-1-84800-165-7 DOI 10.1007/978-1-84800-165-7 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Control Number: 2008923739 © Springer-Verlag London Limited 2008 Apart from any fair dealing for the purposes of research or private study, or criticism or review, as permitted under the Copyright, Designs and Patents Act 1988, this publication may only be reproduced, stored or transmitted, in any form or by any means, with the prior permission in writing of the publishers, or in the case of reprographic reproduction in accordance with the terms of licences issued by the Copyright Licensing Agency. Enquiries concerning reproduction outside those terms should be sent to the publishers. The use of registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant laws and regulations and therefore free for general use. Product liability: The publisher can give no guarantee for information about drug dosage and application thereof contained in this book. -
An Anti-CD6 Monoclonal Antibody (Itolizumab)
Saavedra et al. Immunity & Ageing (2020) 17:34 https://doi.org/10.1186/s12979-020-00207-8 RESEARCH Open Access An anti-CD6 monoclonal antibody (itolizumab) reduces circulating IL-6 in severe COVID-19 elderly patients Danay Saavedra1* , Ana Laura Añé-Kourí2, Naivy Sánchez3, Lázaro Manuel Filgueira4, Julio Betancourt4, Carlos Herrera4, Leniel Manso4, Elibet Chávez5, Armando Caballero4, Carlos Hidalgo3, Geydi Lorenzo1, Meylan Cepeda1, Carmen Valenzuela1, Mayra Ramos1, Kalet León1, Zaima Mazorra1 and Tania Crombet1 Abstract Background: Since the COVID-19 outbreak an unprecedented challenge for healthcare systems around the world has been placed. In Cuba, the first case of COVID-19 was reported on March 11. Elderly with multiple comorbidities have been the most risky population. Although most patients present a mild to moderate disease, some have developed severe symptoms. One of the possible mechanisms underlying rapid disease progression is a cytokine storm, in which interleukin (IL) -6 seems to be a major mediator. Itolizumab is a humanized recombinant anti-CD6 monoclonal antibody (MAb), with the ability of reducing serum interferon gamma (INF-γ), tumour necrosis factor alpha (TNFα) and IL-6. Based on these previous results in patients with psoriasis and rheumatoid arthritis, an expanded access clinical trial was approved by the Cuban regulatory agency for COVID-19 critically, severely and moderately ill patients. Results: We show here a short kinetic of IL-6 serum concentration in the first 24 COVID-19 patients treated with itolizumab. Most of patients were elderly with multiple comorbidities. We found that with one itolizumab dose, the circulating IL-6 decreased in critically and severely ill patients, whereas in moderately ill patients the values didn’t rise as compared to their low baseline levels. -
Histamine in Atopic Disorders: Atopic Dermatitis and Pruritus
Edited by Holger Stark Chapter 6 Histamine in Atopic Disorders: Atopic Dermatitis and Pruritus W. Bäumer1,2, F. Glatzer3, K. Roßbach1, H. Ohtsu4, M. Seike5, S. Mommert3, T. Werfel3, R. Gutzmer3 1Department of Pharmacology, Toxicology and Pharmacy, University of Veterinary Medicine Hannover, 30559 Hannover, Germany 2 Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, USA, e mail: [email protected] 3Division of Immunodermatology and Allergy Research, Hannover Medical School, Germany 4Applied Quantum Medical Engineering, Department of Engineering, Tohoku University, Japan 5Department of Food and Nutrition Science, Sagami Women’s Junior College, Japan 6.1. Role of Histamine and Histamine H4 Receptor in Inflammatory Skin Diseases in Man 6.1.1. Introduction The skin is the primary interface between the environment and the inside of an organism and protects the body against harmful agents, pathogens, allergens, physical trauma, UV radiation and excessive electrolyte and water loss. Different diseases interfere with this function, including the extremely common chronic inflammatory skin diseases. Chronic inflammatory skin diseases are characterized by chronic inflammation of the skin, often with severe pruritus. The most diseases include psoriasis and eczema, including atopic dermatitis (AD) and allergic contact dermatitis (ACD). Numerous different inflammatory cell populations are involved in the pathogenesis of inflammatory skin diseases, including T cells, antigen presenting cells (APC), granulocytes and keratinocytes. The inflamed skin in these diseases becomes dry, red, itchy and scaly, resulting Chapter 6 1 7 3 Histamine H4 Receptor: A Novel Drug Target in Immunoregulation and Inflammation in decreased quality of life. At present, the responsible mechanisms that are involved in inflammation and pruritus in these disorders and how they lead to pathogenesis are not completely understood. -
WO 2016/176089 Al 3 November 2016 (03.11.2016) P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2016/176089 Al 3 November 2016 (03.11.2016) P O P C T (51) International Patent Classification: BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, A01N 43/00 (2006.01) A61K 31/33 (2006.01) DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, (21) International Application Number: KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, MG, PCT/US2016/028383 MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, (22) International Filing Date: PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, SC, 20 April 2016 (20.04.2016) SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (25) Filing Language: English (84) Designated States (unless otherwise indicated, for every (26) Publication Language: English kind of regional protection available): ARIPO (BW, GH, (30) Priority Data: GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, ST, SZ, 62/154,426 29 April 2015 (29.04.2015) US TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, TJ, TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, (71) Applicant: KARDIATONOS, INC. [US/US]; 4909 DK, EE, ES, FI, FR, GB, GR, HR, HU, IE, IS, IT, LT, LU, Lapeer Road, Metamora, Michigan 48455 (US). -
Think Clinical Immunodermatology Laboratory
Clinical ImmunodermatologyThink ImmunodermatologyLaboratory Testing! Kristin M. Leiferman, M.D. Professor of Dermatology Co-Director Immunodermatology Laboratory University of Utah History Late 1800s Paul Ehrlich put forth the concept of autoimmunity calling it “horror autotoxicus” History Early 1940s Albert Coons was the first to conceptualize and develop immunofluorescent techniques for labeling antibodies History 1945 Robin Coombs (and colleagues) described the Coombs antiglobulin reaction test, used to determine if antibodies or complement factors have bound to red blood cell surface antigens in vivo causing hemolytic anemia •Waaler-Rose rheumatoid factor •Hargraves’ LE cell •Witebsky-Rose induction of thyroiditis with autologous thyroid gland History Mid 1960s Ernest Beutner and Robert Jordon demonstrated IgG cell surface antibodies in pemphigus, autoantibodies in circulation and bound to the dermal-epidermal junction in bullous pemphigoid Immunobullous Diseases Immunobullous Diseases • Desmogleins / Desmosomes – Pemphigus • BP Ags in hemidesmosomes / lamina lucida – Pemphigoid – Linear IgA bullous dermatosis • Type VII collagen / anchoring fibrils – Epidermolysis bullosa acquisita Immunodermatology Tests are Diagnostic Aids in Many Diseases • Dermatitis herpetiformis & • Mixed / undefined celiac disease connective tissue disease • Drug reactions • Pemphigoid (all types) • Eosinophil-associated disease • Pemphigus (all types, including paraneoplastic) • Epidermolysis bullosa acquisita • Porphyria & pseudoporphyria • Lichen planus -
Medical Product Quality Report – COVID-19 Issues
Medical Product Quality Report – COVID-19 Issues Issue 9. February 2021 The document has been produced by the Medicine Quality Research Group, Centre of Tropical Medicine & Global Health, Nuffield Department of Medicine, University of Oxford This report was prepared by Kerlijn Van Assche, Céline Caillet and Paul Newton of the Medicine Quality Research Group, that is part of the Infectious Diseases Data Observatory (IDDO) and MORU Tropical Health Network, Centre for Tropical Medicine & Global Health, Nuffield Department of Medicine, University of Oxford, UK. The Globe system was developed by Clark Freifeld (HealthMap, Boston Children’s Hospital, North Eastern University) and Andrew Payne (IDDO), Alberto Olliaro (IDDO) and Gareth Blower (ex-IDDO) with curation of the English reports by Konnie Bellingham, Kitignavong Inthaphavanh and Vayouly Vidhamaly, linked to the Lao- Oxford-Mahosot Hospital-Wellcome Trust Research Unit (LOMWRU), Microbiology Laboratory, Mahosot Hospital, Vientiane, Lao PDR. This document is open access but we would be grateful if you could cite it as: Medicine Quality Research Group, University of Oxford. Medical Product Quality Report – COVID-19 Issues. Issue 9, February 2021. The work is kindly supported by the Bill&Melinda Gates Foundation, the University of Oxford and the Wellcome Trust. March 31th, 2021 2 Contents 1. Summary of findings ........................................................................................... 4 2. Introduction ........................................................................................................ -
William Abramovits, MD
MEDICAL DERMATOLOGY SOCIETY 2020-2021 Mentors WILLIAM ABRAMOVITS, MD Dermatology Treatment & Research Center, Dallas, Texas (P) 972.661.2729 / (E) [email protected] Areas of Expertise: Clinical Research; Eczema; Atopic Dermatitis; Auto-Inflammatory Diseases; Psoriasis LINDSAY SKYE ACKERMAN, MD Medical Dermatology Specialists, PC, Phoenix, Arizona (P) 602.354.5770 / (E) [email protected] Areas of Expertise: Managing Patients with Cutaneous Lymphomas; Severe Psoriasis; Autoimmune Cutaneous Diseases; Collagen Vascular Diseases; Blistering Disorders; Dermatologic Consultations; Clinical Research A RAZZAQUE AHMED, MD/DSC/MPA Center for Blistering Diseases, Boston, Massachusetts (P) 617.562.1040 / (E) [email protected] Areas of Expertise: Autoimmune Blistering Diseases; Comprehensive Approach to Diagnosis and Treatment; Clinical Research; Collaborative Lab Research; Development of Treatment Protocols for New Biologic Agents MILAN ANADKAT, MD Washington University in St. Louis, St. Louis, Missouri (P) 314.362.9859 / (E) [email protected] Areas of Expertise: Chemotherapy Induced Skin Reactions; Dermatologic Therapeutics; Collagen Vascular Disease; Autoimmune Bullous Disease; Graft-versus-Host Disease and Psoriasis DANIEL BACH, MD/MPH University of California, Los Angeles, Los Angeles, California (P) 310.917.3376 / (E) [email protected] Areas of Expertise: Inpatient Dermatology; Oncodermatology; Complex Medical Dermatology JEAN BOLOGNIA, MD Yale University School of Medicine, New Haven, Connecticut (P) 203.785.4092 / (E) -
By Bachelor of Science Oklahoma State University Stillwater
THE ROLE OF KERATINOCYTE DERIVED INTERLEUKIN-1 a AND TUMOR NECROSIS FACTOR a IN EPIDERMAL LANGERHANS CELL DEPLETION By STEPHANIE PICKARD ELIAS Bachelor of Science Oklahoma State University Stillwater, Oklahoma 1993 Bachelor of Science Oklahoma State University Stillwater, Oklahoma 1994 Submitted to the Faculty of the Graduate College of the Oklahoma State University in partial fulfillment of the requirements for the Degree of MASTER OF SCIENCE DECEMBER, 1996 THE ROLE OF KERATfNOCYTE DERIVED INTERLEUKIN-1 a AND TUMOR NECROSIS FACTOR a IN EPIDERMAL LANGERHANS CELL DEPLETION Dean of the Graduate College II PREFACE Advances in the area of skin immunology have been increasing at an explosive rate. With the discovery of skin associated lymphoid tissues and classification of the cells associated wilth this system, much has been learned about how the mammalian body protects itself from invasion by potentially harmful environmental factors. The purpose of this study was to determine, in part, the effect of staphylococcal enterotoxin A (SEA) on cells of the epidermis with regard Langerhans cell migration and cytokine production. This was achieved by Langerhans cell enumeration in murine epidermal sections following exposure to SEA, interleukin-1 a and tumor necrosis factor a through immunohistochemical staining. Results suggested that keratinocyte derived interleukin-1 a and tumor necrosis factor a playa pivotal role in inducing Langerhans cell migration from the skin to the draining lymph node in response to antigenic challenge with SEA. Application of these two cytokines directly to skin sections resulted in depletion of Langerhans cells from the epidermis equivalent to that observed by treatment with SEA.