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Interleukin (IL)-12 and IL-23 and Their Conflicting Roles in Cancer
Downloaded from http://cshperspectives.cshlp.org/ on October 2, 2021 - Published by Cold Spring Harbor Laboratory Press Interleukin (IL)-12 and IL-23 and Their Conflicting Roles in Cancer Juming Yan,1,2 Mark J. Smyth,2,3 and Michele W.L. Teng1,2 1Cancer Immunoregulation and Immunotherapy Laboratory, QIMR Berghofer Medical Research Institute, Herston 4006, Queensland, Australia 2School of Medicine, University of Queensland, Herston 4006, Queensland, Australia 3Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston 4006, Queensland, Australia Correspondence: [email protected] The balance of proinflammatory cytokines interleukin (IL)-12 and IL-23 plays a key role in shaping the development of antitumor or protumor immunity. In this review, we discuss the role IL-12 and IL-23 plays in tumor biology from preclinical and clinical data. In particular, we discuss the mechanism by which IL-23 promotes tumor growth and metastases and how the IL-12/IL-23 axis of inflammation can be targeted for cancer therapy. he recognized interleukin (IL)-12 cytokine composition whereby the a-subunit (p19, Tfamily currently consists of IL-12, IL-23, p28, p35) and b-subunit (p40, Ebi3) are differ- IL-27, and IL-35 and these cytokines play im- entially shared to generate IL-12 (p40-p35), IL- portant roles in the development of appropriate 23 (p40-p19), IL-27 (Ebi3-p28), and IL-35 immune responses in various disease conditions (p40-p35) (Fig. 1A). Given their ability to share (Vignali and Kuchroo 2012). They act as a link a- and b-subunits, it has been predicted that between the innate and adaptive immune system combinations such as Ebi3-p19 and p28-p40 through mediating the appropriate differentia- could exist and serve physiological function tion of naı¨ve CD4þ T cells into various T helper (Fig. -
Genetics of Interleukin 1 Receptor-Like 1 in Immune and Inflammatory Diseases
Current Genomics, 2010, 11, 591-606 591 Genetics of Interleukin 1 Receptor-Like 1 in Immune and Inflammatory Diseases Loubna Akhabir and Andrew Sandford* Department of Medicine, University of British Columbia, UBC James Hogg Research Centre, Providence Heart + Lung Institute, Room 166, St. Paul's Hospital, 1081 Burrard Street, Vancouver, BC V6Z 1Y6, Canada Abstract: Interleukin 1 receptor-like 1 (IL1RL1) is gaining in recognition due to its involvement in immune/inflamma- tory disorders. Well-designed animal studies have shown its critical role in experimental allergic inflammation and human in vitro studies have consistently demonstrated its up-regulation in several conditions such as asthma and rheumatoid ar- thritis. The ligand for IL1RL1 is IL33 which emerged as playing an important role in initiating eosinophilic inflammation and activating other immune cells resulting in an allergic phenotype. An IL1RL1 single nucleotide polymorphism (SNP) was among the most significant results of a genome-wide scan inves- tigating eosinophil counts; in the same study, this SNP associated with asthma in 10 populations. The IL1RL1 gene resides in a region of high linkage disequilibrium containing interleukin 1 receptor genes as well as in- terleukin 18 receptor and accessory genes. This poses a challenge to researchers interested in deciphering genetic associa- tion signals in the region as all of the genes represent interesting candidates for asthma and allergic disease. The IL1RL1 gene and its resulting soluble and receptor proteins have emerged as key regulators of the inflammatory proc- ess implicated in a large variety of human pathologies We review the function and expression of the IL1RL1 gene. -
From IL-15 to IL-33: the Never-Ending List of New Players in Inflammation
From IL-15 to IL-33: the never-ending list of new players in inflammation. Is it time to forget the humble Aspirin and move ahead? Fulvio d’Acquisto, Francesco Maione, Magali Pederzoli-Ribeil To cite this version: Fulvio d’Acquisto, Francesco Maione, Magali Pederzoli-Ribeil. From IL-15 to IL-33: the never-ending list of new players in inflammation. Is it time to forget the humble Aspirin and move ahead?. Bio- chemical Pharmacology, Elsevier, 2009, 79 (4), pp.525. 10.1016/j.bcp.2009.09.015. hal-00544816 HAL Id: hal-00544816 https://hal.archives-ouvertes.fr/hal-00544816 Submitted on 9 Dec 2010 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Accepted Manuscript Title: From IL-15 to IL-33: the never-ending list of new players in inflammation. Is it time to forget the humble Aspirin and move ahead? Authors: Fulvio D’Acquisto, Francesco Maione, Magali Pederzoli-Ribeil PII: S0006-2952(09)00769-2 DOI: doi:10.1016/j.bcp.2009.09.015 Reference: BCP 10329 To appear in: BCP Received date: 30-7-2009 Revised date: 9-9-2009 Accepted date: 10-9-2009 Please cite this article as: D’Acquisto F, Maione F, Pederzoli-Ribeil M, From IL- 15 to IL-33: the never-ending list of new players in inflammation. -
The IL-1-Like Cytokine IL-33 Is Inactivated After Maturation by Caspase-1
The IL-1-like cytokine IL-33 is inactivated after maturation by caspase-1 Corinne Cayrola,b and Jean-Philippe Girarda,b,1 aCentre National de la Recherche Scientifique, Institut de Pharmacologie et de Biologie Structurale, F-31077 Toulouse, France; and bUniversite´de Toulouse, Universite´Paul Sabatier, Institut de Pharmacologie et de Biologie Structurale, F-31077 Toulouse, France Edited by Charles A. Dinarello, University of Colorado Health Sciences Center, Denver, CO, and approved April 10, 2009 (received for review December 13, 2008) IL-33 is a chromatin-associated cytokine of the IL-1 family that has that nuclear IL-33 possesses transcriptional regulatory proper- recently been linked to many diseases, including asthma, rheuma- ties and associates with chromatin in vivo (5). Recently, we found toid arthritis, atherosclerosis, and cardiovascular diseases. IL-33 that IL-33 mimics Kaposi sarcoma herpesvirus for attachment to signals through the IL-1 receptor-related protein ST2 and drives chromatin, and docks, through a short chromatin-binding pep- production of pro-inflammatory and T helper type 2-associated tide, into the acidic pocket formed by the histone H2A-H2B cytokines in mast cells, T helper type 2 lymphocytes, basophils, dimer at the surface of the nucleosome (22). Together, our eosinophils, invariant natural killer T cells, and natural killer cells. findings suggested IL-33 is a dual-function protein that may play It is currently believed that IL-33, like IL-1 and IL-18, requires important roles as both a cytokine and an intracellular nuclear processing by caspase-1 to a mature form (IL-33112–270) for biolog- factor (5, 22). -
Genetic Determinants of Circulating Interleukin-1 Receptor Antagonist Levels and Their Association with Glycemic Traits
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Trepo - Institutional Repository of Tampere University GENETIC DETERMINANTS OF CIRCULATING INTERLEUKIN-1 RECEPTOR ANTAGONIST LEVELS AND THEIR ASSOCIATION WITH GLYCEMIC TRAITS Marja-Liisa Nuotio Syventävien opintojen kirjallinen työ Tampereen yliopisto Lääketieteen yksikkö Tammikuu 2015 Tampereen yliopisto Lääketieteen yksikkö NUOTIO MARJA-LIISA: GENETIC DETERMINANTS OF CIRCULATING INTERLEUKIN-1 RECEPTOR ANTAGONIST LEVELS AND THEIR ASSOCIATION WITH GLYCEMIC TRAITS Kirjallinen työ, 57 s. Ohjaaja: professori Mika Kähönen Tammikuu 2015 Avainsanat: sytokiinit, insuliiniresistenssi, tyypin 2 diabetes, tulehdus, glukoosimetabolia, genominlaajuinen assosiaatioanalyysi (GWAS) Tulehdusta välittäviin sytokiineihin kuuluvan interleukiini 1β (IL-1β):n kohonneen systeemisen pitoisuuden on arveltu edesauttavan insuliiniresistenssin kehittymistä ja johtavan haiman β-solujen toimintahäiriöihin. IL-1β:n sisäsyntyisellä vastavaikuttajalla, interleukiini 1 reseptoriantagonistilla (IL-1RA), on puolestaan esitetty olevan suojaava rooli mainittujen fenotyyppien kehittymisessä päinvastaisten vaikutustensa ansiosta. IL-1RA:n suojaavan roolin havainnollistamiseksi työssä Genetic determinants of circulating interleukin-1 receptor antagonist levels and their association with glycemic traits tunnistettiin veren IL-1RA- pitoisuuteen assosioituvia geneettisiä variantteja, minkä jälkeen selvitettiin näiden yhteyttä glukoosi- ja insuliinimetaboliaan liittyvien muuttujien-, sekä -
Interleukin-18 As a Therapeutic Target in Acute Myocardial Infarction and Heart Failure
Interleukin-18 as a Therapeutic Target in Acute Myocardial Infarction and Heart Failure Laura C O’Brien,1 Eleonora Mezzaroma,2,3,4 Benjamin W Van Tassell,2,3,4 Carlo Marchetti,2,3 Salvatore Carbone,2,3 Antonio Abbate,1,2,3 and Stefano Toldo2,3 1Department of Physiology and Biophysics, 2Victoria Johnson Research Laboratories, and 3Virginia Commonwealth University Pauley Heart Center, School of Medicine, and 4Pharmacotherapy and Outcome Sciences, School of Pharmacy, Virginia Commonwealth University, Richmond, Virginia, United States of America Interleukin 18 (IL-18) is a proinflammatory cytokine in the IL-1 family that has been implicated in a number of disease states. In animal models of acute myocardial infarction (AMI), pressure overload, and LPS-induced dysfunction, IL-18 regulates cardiomy- ocyte hypertrophy and induces cardiac contractile dysfunction and extracellular matrix remodeling. In patients, high IL-18 levels correlate with increased risk of developing cardiovascular disease (CVD) and with a worse prognosis in patients with established CVD. Two strategies have been used to counter the effects of IL-18:IL-18 binding protein (IL-18BP), a naturally occurring protein, and a neutralizing IL-18 antibody. Recombinant human IL-18BP (r-hIL-18BP) has been investigated in animal studies and in phase I/II clinical trials for psoriasis and rheumatoid arthritis. A phase II clinical trial using a humanized monoclonal IL-18 antibody for type 2 diabetes is ongoing. Here we review the literature regarding the role of IL-18 in AMI and heart failure and the evidence and challenges of using IL-18BP and blocking IL-18 antibodies as a therapeutic strategy in patients with heart disease. -
Interleukin-33 Signaling Exacerbates Experimental Infectious Colitis by Enhancing Gut Permeability and Inhibiting Protective Th17 Immunity
www.nature.com/mi ARTICLE OPEN Interleukin-33 signaling exacerbates experimental infectious colitis by enhancing gut permeability and inhibiting protective Th17 immunity Vittoria Palmieri1, Jana-Fabienne Ebel1, Nhi Ngo Thi Phuong1, Robert Klopfleisch2, Vivian Pham Vu3,4, Alexandra Adamczyk1, Julia Zöller1, Christian Riedel5, Jan Buer1, Philippe Krebs3, Wiebke Hansen1, Eva Pastille1 and Astrid M. Westendorf 1 A wide range of microbial pathogens is capable of entering the gastrointestinal tract, causing infectious diarrhea and colitis. A finely tuned balance between different cytokines is necessary to eradicate the microbial threat and to avoid infection complications. The current study identified IL-33 as a critical regulator of the immune response to the enteric pathogen Citrobacter rodentium.We observed that deficiency of the IL-33 signaling pathway attenuates bacterial-induced colitis. Conversely, boosting this pathway strongly aggravates the inflammatory response and makes the mice prone to systemic infection. Mechanistically, IL-33 mediates its detrimental effect by enhancing gut permeability and by limiting the induction of protective T helper 17 cells at the site of infection, thus impairing host defense mechanisms against the enteric pathogen. Importantly, IL-33-treated infected mice supplemented with IL-17A are able to resist the otherwise strong systemic spreading of the pathogen. These findings reveal a novel IL-33/IL-17A crosstalk that controls the pathogenesis of Citrobacter rodentium-driven infectious colitis. Manipulating the dynamics of cytokines may offer new therapeutic strategies to treat specific intestinal infections. 1234567890();,: Mucosal Immunology (2021) 14:923–936; https://doi.org/10.1038/s41385-021-00386-7 INTRODUCTION epithelial cells, and endothelial cells in response to injury6. -
Cellular and Molecular Signatures in the Disease Tissue of Early
Cellular and Molecular Signatures in the Disease Tissue of Early Rheumatoid Arthritis Stratify Clinical Response to csDMARD-Therapy and Predict Radiographic Progression Frances Humby1,* Myles Lewis1,* Nandhini Ramamoorthi2, Jason Hackney3, Michael Barnes1, Michele Bombardieri1, Francesca Setiadi2, Stephen Kelly1, Fabiola Bene1, Maria di Cicco1, Sudeh Riahi1, Vidalba Rocher-Ros1, Nora Ng1, Ilias Lazorou1, Rebecca E. Hands1, Desiree van der Heijde4, Robert Landewé5, Annette van der Helm-van Mil4, Alberto Cauli6, Iain B. McInnes7, Christopher D. Buckley8, Ernest Choy9, Peter Taylor10, Michael J. Townsend2 & Costantino Pitzalis1 1Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Departments of 2Biomarker Discovery OMNI, 3Bioinformatics and Computational Biology, Genentech Research and Early Development, South San Francisco, California 94080 USA 4Department of Rheumatology, Leiden University Medical Center, The Netherlands 5Department of Clinical Immunology & Rheumatology, Amsterdam Rheumatology & Immunology Center, Amsterdam, The Netherlands 6Rheumatology Unit, Department of Medical Sciences, Policlinico of the University of Cagliari, Cagliari, Italy 7Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK 8Rheumatology Research Group, Institute of Inflammation and Ageing (IIA), University of Birmingham, Birmingham B15 2WB, UK 9Institute of -
The Role of Interleukin-36 in Inflammatory Skin Diseases
UNIVERSITÀ DEGLI STUDI DI NAPOLI FEDERICO II DOTTORATO DI RICERCA IN MEDICINA CLINICA E SPERIMENTALE CURRICULUM IN SCIENZE IMMUNOLOGICHE E DERMATOLOGICHE XXIX Ciclo Coordinatore: Prof. Gianni Marone TESI DI DOTTORATO TITOLO The role of interleukin-36 in inflammatory skin diseases TUTOR/RELATORE CANDIDATA Chiar.mo Dott.ssa Giuseppina Caiazzo Prof. Fabio Ayala INDEX Summary .…………………………………………………………. page 2 I CHAPTER IL-36 cytokines……………………………………………………... page 3 IL-36 and their immune function………………………………….. page 5 II CHAPTER IL-36 and diseases…………………………………………………… page 7 IL-36 and skin diseases……………………………………………… page 7 Pathogenesis of psoriasis …………………………………………… page 9 Pathogenesis of allergic contact dermatitis………………………… page 12 Pathogenesis of polymorphic light eruption..………………………. page14 III CHAPTER Experimental Design………………………………………………..... page 17 Materials and methods........................................................................ page 17 Results……………………………………………………………….... page 24 VI CHAPTER Discussion……………………………………………………………… page 31 References 1 Summary Interleukin (IL)-36 cytokines are new members of the IL-1 family, that include pro- inflammatory factors, IL-36α, IL-36β and IL-36γ, and a natural receptor antagonist IL-36Ra. IL-36 cytokines are expressed in a specific manner by monocytes/macrophages, dendritic cells (DCs), T cells subsets, keratinocytes, Langerhans cells, and mucosal epithelium. Since IL-36 cytokines are predominantly expressed in keratinocytes it is not surprising that specifically skin disorders have been -
Inflammation-Induced IL-6 Functions As a Natural Brake On
BASIC RESEARCH www.jasn.org Inflammation-Induced IL-6 Functions as a Natural Brake on Macrophages and Limits GN Michael Luig,* Malte A. Kluger,* Boeren Goerke,* Matthias Meyer,* Anna Nosko,* † ‡ † Isabell Yan, Jürgen Scheller, Hans-Willi Mittrücker, Stefan Rose-John,§ Rolf A.K. Stahl,* Ulf Panzer,* and Oliver M. Steinmetz* *Medical Clinic III and †Immunology Institute, Hamburg University Medical Center, Hamburg, Germany; ‡Institute of Biochemistry and Molecular Biology II, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany; and §Institute of Biochemistry, Christian-Albrechts-University, Kiel, Germany ABSTRACT IL-6 can mediate proinflammatory effects, and IL-6 receptor (IL-6R) blockade as a treatment for in- flammatory diseases has entered clinical practice. However, opposing effects of IL-6 have been observed in models of GN. Although IL-6 is proinflammatory in murine lupus nephritis, protective effects have been observed for IL-6 in the nephrotoxic nephritis (NTN) model of acute crescentic GN. In light of the potential dangers of IL-6–directed treatment, we studied the mechanisms underlying the contradictory findings in GN. IL-6 can signal through the membrane-bound IL-6R, which is expressed only on hepatocytes and certain leukocytes (classic), or through the soluble IL-6R, which binds the ubiquitously expressed gp130 (alternative). Preemptive treatment of mice with anti-IL-6R or anti-IL-6 worsened NTN, whereas selective blockade of alternative IL-6 signaling by the fusion protein sgp130Fc did not. FACS analysis of mouse spleen cells revealed proinflammatory macrophages express the highest levels of IL-6Ra,andin vitro treatment with IL-6 blocked macrophage proliferation. Furthermore, proinflammatory macrophages were 2 2 expanded during inflammation in IL-6 / mice. -
T Cell–Derived IL-22 Amplifies IL-1B–Driven Inflammation in Human Adipose Tissue
1966 Diabetes Volume 63, June 2014 Elise Dalmas,1,2,3,4 Nicolas Venteclef,1,2,3,4 Charles Caer,1,2,3,4 Christine Poitou,1,2,3,4,5 Isabelle Cremer,1,2,3 Judith Aron-Wisnewsky,1,2,3,4,5 Sébastien Lacroix-Desmazes,1,2,3 Jagadeesh Bayry,1,2,3 Srinivas V. Kaveri,1,2,3 Karine Clément,1,2,3,4,5 Sébastien André,1,2,3,4 and Michèle Guerre-Millo1,2,3,4 T Cell–Derived IL-22 Amplifies IL-1b–Driven Inflammation in Human Adipose Tissue: Relevance to Obesity and Type 2 Diabetes Diabetes 2014;63:1966–1977 | DOI: 10.2337/db13-1511 Proinflammatory cytokines are critically involved in the combined anti-IL-1b and anti-IL-22 immunotherapy alteration of adipose tissue biology leading to deteri- in human obesity. oration of glucose homeostasis in obesity. Here we show a pronounced proinflammatory signature of adi- pose tissue macrophages in type 2 diabetic obese pa- A causal relationship between macrophage accumulation in tients, mainly driven by increased NLRP3-dependent adipose tissue and systemic insulin resistance has been interleukin (IL)-1b production. IL-1b release increased clearly established in mouse studies, in which macrophage with glycemic deterioration and decreased after gas- abundance can be manipulated through diet, genetic, or tric bypass surgery. A specific enrichment of IL-17- pharmacological intervention (1–3). In humans, however, + OBESITY STUDIES and IL-22-producing CD4 T cells was found in adipose the amount of adipose tissue macrophages is not consis- tissue of type 2 diabetic obese patients. -
The Interleukin 22 Pathway Interacts with Mutant KRAS to Promote Poor Prognosis in Colon Cancer
Author Manuscript Published OnlineFirst on May 19, 2020; DOI: 10.1158/1078-0432.CCR-19-1086 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. The interleukin 22 pathway interacts with mutant KRAS to promote poor prognosis in colon cancer Authors: Sarah McCuaig1, David Barras,2, Elizabeth Mann1, Matthias Friedrich1, Samuel Bullers1, Alina Janney1, Lucy C. Garner1, Enric Domingo3, Viktor Hendrik Koelzer3,4,5, Mauro Delorenzi2,6,7, Sabine Tejpar8, Timothy Maughan9, Nathaniel R. West1, Fiona Powrie1 Affiliations: 1 Kennedy Institute of Rheumatology, University of Oxford, Oxford UK. 2 SIB Swiss Institute of Bioinformatics, Bioinformatics Core Facility, Lausanne, Switzerland. 3Department of Oncology, University of Oxford, Oxford UK. 4Nuffield Department of Medicine, University of Oxford, Oxford UK. 5Department of Pathology and Molecular Pathology, University and University Hospital Zurich, Zurich Switzerland. 6 Ludwig Center for Cancer Research, University of Lausanne, Lausanne, Switzerland. 7 Department of Oncology, Faculty of Biology and Medicine, University of Lausanne, Lausanne Switzerland. 8 Molecular Digestive Oncology, KU Leuven, Belgium. 9 CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Oxford, UK. Downloaded from clincancerres.aacrjournals.org on September 26, 2021. © 2020 American Association for Cancer Research. Author Manuscript Published OnlineFirst on May 19, 2020; DOI: 10.1158/1078-0432.CCR-19-1086 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Correspondence to: Professor Fiona Powrie; Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, Headington, Oxford, OX3 7YF, UK. Email: [email protected] Conflicts of Interest: S.M., N.R.W., and F.P.