Microbiota-Dependent Effects of IL-22
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IL-22 Binding Protein Promotes the Disease Process in Multiple Sclerosis Hannes Lindahl, André O
IL-22 Binding Protein Promotes the Disease Process in Multiple Sclerosis Hannes Lindahl, André O. Guerreiro-Cacais, Sahl Khalid Bedri, Mathias Linnerbauer, Magdalena Lindén, Nada This information is current as Abdelmagid, Karolina Tandre, Claire Hollins, Lorraine of September 24, 2021. Irving, Colin Glover, Clare Jones, Lars Alfredsson, Lars Rönnblom, Ingrid Kockum, Mohsen Khademi, Maja Jagodic and Tomas Olsson J Immunol published online 10 July 2019 Downloaded from http://www.jimmunol.org/content/early/2019/07/09/jimmun ol.1900400 Supplementary http://www.jimmunol.org/content/suppl/2019/07/10/jimmunol.190040 http://www.jimmunol.org/ Material 0.DCSupplemental Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 24, 2021 • Fast Publication! 4 weeks from acceptance to publication *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 © 2019 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published -
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. -
Mice in Inflammation Psoriasiform Skin IL-22 Is Required for Imiquimod-Induced
IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice Astrid B. Van Belle, Magali de Heusch, Muriel M. Lemaire, Emilie Hendrickx, Guy Warnier, Kyri This information is current as Dunussi-Joannopoulos, Lynette A. Fouser, Jean-Christophe of September 29, 2021. Renauld and Laure Dumoutier J Immunol published online 30 November 2011 http://www.jimmunol.org/content/early/2011/11/30/jimmun ol.1102224 Downloaded from Why The JI? Submit online. http://www.jimmunol.org/ • 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 *average by guest on September 29, 2021 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. Published November 30, 2011, doi:10.4049/jimmunol.1102224 The Journal of Immunology IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice Astrid B. Van Belle,*,† Magali de Heusch,*,† Muriel M. Lemaire,*,† Emilie Hendrickx,*,† Guy Warnier,*,† Kyri Dunussi-Joannopoulos,‡ Lynette A. Fouser,‡ Jean-Christophe Renauld,*,†,1 and Laure Dumoutier*,†,1 Psoriasis is a common chronic autoimmune skin disease of unknown cause that involves dysregulated interplay between immune cells and keratinocytes. -
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. -
Igs Cells Recognize Bacteria with Polyreactive Memory B +Iga
Circulating Human CD27−IgA+ Memory B Cells Recognize Bacteria with Polyreactive Igs This information is current as Magdalena A. Berkowska, Jean-Nicolas Schickel, Christina of October 2, 2021. Grosserichter-Wagener, Dick de Ridder, Yen Shing Ng, Jacques J. M. van Dongen, Eric Meffre and Menno C. van Zelm J Immunol 2015; 195:1417-1426; Prepublished online 6 July 2015; doi: 10.4049/jimmunol.1402708 Downloaded from http://www.jimmunol.org/content/195/4/1417 Supplementary http://www.jimmunol.org/content/suppl/2015/07/03/jimmunol.140270 http://www.jimmunol.org/ Material 8.DCSupplemental References This article cites 57 articles, 31 of which you can access for free at: http://www.jimmunol.org/content/195/4/1417.full#ref-list-1 Why The JI? Submit online. by guest on October 2, 2021 • 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 *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 © 2015 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Circulating Human CD272IgA+ Memory B Cells Recognize Bacteria with Polyreactive Igs Magdalena A. -
1714 Gene Comprehensive Cancer Panel Enriched for Clinically Actionable Genes with Additional Biologically Relevant Genes 400-500X Average Coverage on Tumor
xO GENE PANEL 1714 gene comprehensive cancer panel enriched for clinically actionable genes with additional biologically relevant genes 400-500x average coverage on tumor Genes A-C Genes D-F Genes G-I Genes J-L AATK ATAD2B BTG1 CDH7 CREM DACH1 EPHA1 FES G6PC3 HGF IL18RAP JADE1 LMO1 ABCA1 ATF1 BTG2 CDK1 CRHR1 DACH2 EPHA2 FEV G6PD HIF1A IL1R1 JAK1 LMO2 ABCB1 ATM BTG3 CDK10 CRK DAXX EPHA3 FGF1 GAB1 HIF1AN IL1R2 JAK2 LMO7 ABCB11 ATR BTK CDK11A CRKL DBH EPHA4 FGF10 GAB2 HIST1H1E IL1RAP JAK3 LMTK2 ABCB4 ATRX BTRC CDK11B CRLF2 DCC EPHA5 FGF11 GABPA HIST1H3B IL20RA JARID2 LMTK3 ABCC1 AURKA BUB1 CDK12 CRTC1 DCUN1D1 EPHA6 FGF12 GALNT12 HIST1H4E IL20RB JAZF1 LPHN2 ABCC2 AURKB BUB1B CDK13 CRTC2 DCUN1D2 EPHA7 FGF13 GATA1 HLA-A IL21R JMJD1C LPHN3 ABCG1 AURKC BUB3 CDK14 CRTC3 DDB2 EPHA8 FGF14 GATA2 HLA-B IL22RA1 JMJD4 LPP ABCG2 AXIN1 C11orf30 CDK15 CSF1 DDIT3 EPHB1 FGF16 GATA3 HLF IL22RA2 JMJD6 LRP1B ABI1 AXIN2 CACNA1C CDK16 CSF1R DDR1 EPHB2 FGF17 GATA5 HLTF IL23R JMJD7 LRP5 ABL1 AXL CACNA1S CDK17 CSF2RA DDR2 EPHB3 FGF18 GATA6 HMGA1 IL2RA JMJD8 LRP6 ABL2 B2M CACNB2 CDK18 CSF2RB DDX3X EPHB4 FGF19 GDNF HMGA2 IL2RB JUN LRRK2 ACE BABAM1 CADM2 CDK19 CSF3R DDX5 EPHB6 FGF2 GFI1 HMGCR IL2RG JUNB LSM1 ACSL6 BACH1 CALR CDK2 CSK DDX6 EPOR FGF20 GFI1B HNF1A IL3 JUND LTK ACTA2 BACH2 CAMTA1 CDK20 CSNK1D DEK ERBB2 FGF21 GFRA4 HNF1B IL3RA JUP LYL1 ACTC1 BAG4 CAPRIN2 CDK3 CSNK1E DHFR ERBB3 FGF22 GGCX HNRNPA3 IL4R KAT2A LYN ACVR1 BAI3 CARD10 CDK4 CTCF DHH ERBB4 FGF23 GHR HOXA10 IL5RA KAT2B LZTR1 ACVR1B BAP1 CARD11 CDK5 CTCFL DIAPH1 ERCC1 FGF3 GID4 HOXA11 IL6R KAT5 ACVR2A -
Evolutionary Divergence and Functions of the Human Interleukin (IL) Gene Family Chad Brocker,1 David Thompson,2 Akiko Matsumoto,1 Daniel W
UPDATE ON GENE COMPLETIONS AND ANNOTATIONS Evolutionary divergence and functions of the human interleukin (IL) gene family Chad Brocker,1 David Thompson,2 Akiko Matsumoto,1 Daniel W. Nebert3* and Vasilis Vasiliou1 1Molecular Toxicology and Environmental Health Sciences Program, Department of Pharmaceutical Sciences, University of Colorado Denver, Aurora, CO 80045, USA 2Department of Clinical Pharmacy, University of Colorado Denver, Aurora, CO 80045, USA 3Department of Environmental Health and Center for Environmental Genetics (CEG), University of Cincinnati Medical Center, Cincinnati, OH 45267–0056, USA *Correspondence to: Tel: þ1 513 821 4664; Fax: þ1 513 558 0925; E-mail: [email protected]; [email protected] Date received (in revised form): 22nd September 2010 Abstract Cytokines play a very important role in nearly all aspects of inflammation and immunity. The term ‘interleukin’ (IL) has been used to describe a group of cytokines with complex immunomodulatory functions — including cell proliferation, maturation, migration and adhesion. These cytokines also play an important role in immune cell differentiation and activation. Determining the exact function of a particular cytokine is complicated by the influence of the producing cell type, the responding cell type and the phase of the immune response. ILs can also have pro- and anti-inflammatory effects, further complicating their characterisation. These molecules are under constant pressure to evolve due to continual competition between the host’s immune system and infecting organisms; as such, ILs have undergone significant evolution. This has resulted in little amino acid conservation between orthologous proteins, which further complicates the gene family organisation. Within the literature there are a number of overlapping nomenclature and classification systems derived from biological function, receptor-binding properties and originating cell type. -
Metamorphic Protein Folding Encodes Multiple Anti-Candida Mechanisms in XCL1
pathogens Article Metamorphic Protein Folding Encodes Multiple Anti-Candida Mechanisms in XCL1 Acacia F. Dishman 1,2,†, Jie He 3,†, Brian F. Volkman 1,* and Anna R. Huppler 3,* 1 Department of Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, USA; [email protected] 2 Medical Scientist Training Program, Medical College of Wisconsin, Milwaukee, WI 53226, USA 3 Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226, USA; [email protected] * Correspondence: [email protected] (B.F.V.); [email protected] (A.R.H.) † These authors contributed equally. Abstract: Candida species cause serious infections requiring prolonged and sometimes toxic therapy. Antimicrobial proteins, such as chemokines, hold great interest as potential additions to the small number of available antifungal drugs. Metamorphic proteins reversibly switch between multiple different folded structures. XCL1 is a metamorphic, antimicrobial chemokine that interconverts between the conserved chemokine fold (an α–β monomer) and an alternate fold (an all-β dimer). Previous work has shown that human XCL1 kills C. albicans but has not assessed whether one or both XCL1 folds perform this activity. Here, we use structurally locked engineered XCL1 variants and Candida killing assays, adenylate kinase release assays, and propidium iodide uptake assays to demonstrate that both XCL1 folds kill Candida, but they do so via different mechanisms. Our results suggest that the alternate fold kills via membrane disruption, consistent with previous work, and the chemokine fold does not. XCL1 fold-switching thus provides a mechanism to regulate Citation: Dishman, A.F.; He, J.; the XCL1 mode of antifungal killing, which could protect surrounding tissue from damage associ- Volkman, B.F.; Huppler, A.R. -
Wound-Healing Markers Revealed by Proximity Extension Assay in Tears of Patients Following Glaucoma Surgery
International Journal of Molecular Sciences Article Wound-Healing Markers Revealed by Proximity Extension Assay in Tears of Patients following Glaucoma Surgery Éva Cs˝osz 1,2,* , Noémi Tóth 3, Eszter Deák 1,3, Adrienne Csutak 3,† and József T˝ozsér 1,2,† 1 Biomarker Research Group, Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Egyetem ter 1., 4032 Debrecen, Hungary; [email protected] (E.D.); [email protected] (J.T.) 2 Proteomics Core Facility, Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Egyetem ter 1., 4032 Debrecen, Hungary 3 Department of Ophthalmology, Faculty of Medicine, University of Debrecen, Nagyerdei krt. 98., 4032 Debrecen, Hungary; [email protected] (N.T.); [email protected] (A.C.) * Correspondence: [email protected]; Tel.: +36-52-416-432 † These authors contributed equally to this work. Received: 15 October 2018; Accepted: 11 December 2018; Published: 18 December 2018 Abstract: Tears are a constantly available and highly valuable body fluid collectable by non-invasive techniques. Although it can give information on ocular status and be used for follow-ups, tear analysis is challenging due to the low amount of sample that is available. Proximity extension assay (PEA) allows for a sensitive and scalable analysis of multiple proteins in a single run from a one-µL sample, so we applied this technique and examined the amount of 184 proteins in tears collected at different time points after trabeculectomy. The success rate of this surgical intervention highly depends on proper wound healing; therefore, information on the process is indispensable. -
Th22 Cells Represent a Distinct Human T Cell Subset Involved in Epidermal Immunity and Remodeling
Th22 cells represent a distinct human T cell subset involved in epidermal immunity and remodeling Stefanie Eyerich, … , Carsten B. Schmidt-Weber, Andrea Cavani J Clin Invest. 2009;119(12):3573-3585. https://doi.org/10.1172/JCI40202. Research Article Immunology Th subsets are defined according to their production of lineage-indicating cytokines and functions. In this study, we have identified a subset of human Th cells that infiltrates the epidermis in individuals with inflammatory skin disorders and is characterized by the secretion of IL-22 and TNF-α, but not IFN-γ, IL-4, or IL-17. In analogy to the Th17 subset, cells with this cytokine profile have been named the Th22 subset. Th22 clones derived from patients with psoriasis were stable in culture and exhibited a transcriptome profile clearly separate from those of Th1, Th2, and Th17 cells; it included genes encoding proteins involved in tissue remodeling, such as FGFs, and chemokines involved in angiogenesis and fibrosis. Primary human keratinocytes exposed to Th22 supernatants expressed a transcriptome response profile that included genes involved in innate immune pathways and the induction and modulation of adaptive immunity. These proinflammatory Th22 responses were synergistically dependent on IL-22 and TNF-α. Furthermore, Th22 supernatants enhanced wound healing in an in vitro injury model, which was exclusively dependent on IL-22. In conclusion, the human Th22 subset may represent a separate T cell subset with a distinct identity with respect to gene expression and function, present within the epidermal layer in inflammatory skin diseases. Future strategies directed against the Th22 subset may be of value in chronic inflammatory skin disorders. -
Development and Validation of a Protein-Based Risk Score for Cardiovascular Outcomes Among Patients with Stable Coronary Heart Disease
Supplementary Online Content Ganz P, Heidecker B, Hveem K, et al. Development and validation of a protein-based risk score for cardiovascular outcomes among patients with stable coronary heart disease. JAMA. doi: 10.1001/jama.2016.5951 eTable 1. List of 1130 Proteins Measured by Somalogic’s Modified Aptamer-Based Proteomic Assay eTable 2. Coefficients for Weibull Recalibration Model Applied to 9-Protein Model eFigure 1. Median Protein Levels in Derivation and Validation Cohort eTable 3. Coefficients for the Recalibration Model Applied to Refit Framingham eFigure 2. Calibration Plots for the Refit Framingham Model eTable 4. List of 200 Proteins Associated With the Risk of MI, Stroke, Heart Failure, and Death eFigure 3. Hazard Ratios of Lasso Selected Proteins for Primary End Point of MI, Stroke, Heart Failure, and Death eFigure 4. 9-Protein Prognostic Model Hazard Ratios Adjusted for Framingham Variables eFigure 5. 9-Protein Risk Scores by Event Type This supplementary material has been provided by the authors to give readers additional information about their work. Downloaded From: https://jamanetwork.com/ on 10/02/2021 Supplemental Material Table of Contents 1 Study Design and Data Processing ......................................................................................................... 3 2 Table of 1130 Proteins Measured .......................................................................................................... 4 3 Variable Selection and Statistical Modeling ........................................................................................