(12) Patent Application Publication (10) Pub. No.: US 2016/0367695A1 Wilson Et Al
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Correlation of Cytokine Level with the Severity of Severe Fever With
Liu et al. Virology Journal (2017) 14:6 DOI 10.1186/s12985-016-0677-1 RESEARCH Open Access Correlation of cytokine level with the severity of severe fever with thrombocytopenia syndrome Miao-Miao Liu1, Xiao-Ying Lei1, Hao Yu2, Jian-zhi Zhang3 and Xue-jie Yu1,4* Abstract Background: Severe fever with thrombocytopenia syndrome (SFTS) was an emerging hemorrhagic fever that was caused by a tick-borne bunyavirus, SFTSV. Although SFTSV nonstructural protein can inhibit type I interferon (IFN-I) production Ex Vivo and IFN-I played key role in resistance SFTSV infection in animal model, the role of IFN-I in patients is not investigated. Methods: We have assayed the concentration of IFN-α, a subtype of IFN-I as well as other cytokines in the sera of SFTS patients and the healthy population with CBA (Cytometric bead array) assay. Results: The results showed that IFN-α, tumor necrosis factor (TNF-α), granulocyte colony-stimulating factor (G-CSF), interferon-γ (IFN-γ), macrophage inflammatory protein (MIP-1α), interleukin-6 (IL-6), IL-10, interferon-inducible protein (IP-10), monocyte chemoattractant protein (MCP-1) were significantly higher in SFTS patients than in healthy persons (p < 0.05); the concentrations of IFN-α, IFN-γ, G-CSF, MIP-1α, IL-6, and IP-10 were significant higher in severe SFTS patients than in mild SFTS patients (p < 0.05). Conclusion: The concentration of IFN-α as well as other cytokines (IFN-γ, G-CSF, MIP-1α, IL-6, and IP-10) is correlated with the severity of SFTS, suggesting that type I interferon may not be significant in resistance SFTSV infection in humans and it may play an import role in cytokine storm. -
Accepted Manuscript
Lawrence Berkeley National Laboratory Recent Work Title CVID enteropathy is characterized by exceeding low mucosal IgA levels and interferon- driven inflammation possibly related to the presence of a pathobiont. Permalink https://escholarship.org/uc/item/7qv434pj Authors Shulzhenko, Natalia Dong, Xiaoxi Vyshenska, Dariia et al. Publication Date 2018-12-01 DOI 10.1016/j.clim.2018.09.008 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Accepted Manuscript CVID enteropathy is characterized by exceeding low mucosal iga levels and interferon-driven inflammation possibly related to the presence of a pathobiont Natalia Shulzhenko, Xiaoxi Dong, Dariia Vyshenska, Renee L. Greer, Manoj Gurung, Stephany Vasquez-Perez, Ekaterina Peremyslova, Stanislav Sosnovtsev, Martha Quezado, Michael Yao, Kim Montgomery-Recht, Warren Strober, Ivan J. Fuss, Andrey Morgun PII: S1521-6616(18)30294-8 DOI: doi:10.1016/j.clim.2018.09.008 Reference: YCLIM 8102 To appear in: Clinical Immunology Received date: 25 April 2018 Revised date: 2 August 2018 Accepted date: 16 September 2018 Please cite this article as: Natalia Shulzhenko, Xiaoxi Dong, Dariia Vyshenska, Renee L. Greer, Manoj Gurung, Stephany Vasquez-Perez, Ekaterina Peremyslova, Stanislav Sosnovtsev, Martha Quezado, Michael Yao, Kim Montgomery-Recht, Warren Strober, Ivan J. Fuss, Andrey Morgun , CVID enteropathy is characterized by exceeding low mucosal iga levels and interferon-driven inflammation possibly related to the presence of a pathobiont. Yclim (2018), doi:10.1016/j.clim.2018.09.008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. -
WO 2010/142017 Al
(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 16 December 2010 (16.12.2010) WO 2010/142017 Al (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61K 48/00 (2006.01) A61P 37/04 (2006.01) kind of national protection available): AE, AG, AL, AM, A61P 31/00 (2006.01) A61K 38/21 (2006.01) AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, (21) Number: International Application DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, PCT/CA20 10/000844 HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, (22) International Filing Date: KR, KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, 8 June 2010 (08.06.2010) ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, PE, PG, PH, PL, PT, RO, RS, RU, SC, SD, (25) Filing Language: English SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, (26) Publication Language: English TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (30) Priority Data: (84) Designated States (unless otherwise indicated, for every 61/185,261 9 June 2009 (09.06.2009) US kind of regional protection available): ARIPO (BW, GH, GM, KE, LR, LS, MW, MZ, NA, SD, SL, SZ, TZ, UG, (71) Applicant (for all designated States except US): DE- ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, MD, RU, TJ, FYRUS, INC . -
( 12 ) Patent Application Publication ( 10 ) Pub . No .: US 2020/0331966 A1 STOVER Et Al
US 20200331966A1 IN ( 19 ) United States ( 12 ) Patent Application Publication ( 10 ) Pub . No .: US 2020/0331966 A1 STOVER et al . ( 43 ) Pub . Date : Oct. 22 , 2020 ( 54 ) FUSION PROTEIN COMPOSITION ( S ) Related U.S. Application Data COMPRISING MASKED TYPE I INTERFERONS ( IFNA AND IFNB ) FOR USE ( 60 ) Provisional application No. 62 / 920,140 , filed on Apr. IN THE TREATMENT OF CANCER AND 15 , 2019 . METHODS THEREOF Publication Classification ( 71 ) Applicant: Qwixel Therapeutics, Los Angeles, CA ( 51 ) Int. Ci . ( US ) CO7K 7/08 ( 2006.01 ) A61K 47/65 ( 2006.01 ) ( 72 ) Inventors : David STOVER , Encino, CA (US ) ; A61P 35/00 ( 2006.01 ) Sherie MORRISON , Los Angeles, CA ( 52 ) U.S. CI . ( US ) ; Alex VASUTHASAWAT , Los CPC CO7K 7/08 ( 2013.01 ) ; A61K 38/00 Angeles , CA ( US ) ; Kham TRINH , ( 2013.01 ) ; A61P 35/00 ( 2018.01 ) ; A61K 47/65 Porter Ranch , CA ( US ) ; George ( 2017.08 ) AYOUB , Los Angeles, CA ( US ) ( 57 ) ABSTRACT Fusion Protein compositions comprising masked IFNs and ( 73 ) Assignee : Qwixel Therapeutics, Los Angeles, CA methods of making masked IFNs are disclosed herein . ( US ) Consequently, the masked IFNs can be fused to a Mab or binding fragment thereof and be administered to patients as ( 21 ) Appl. No .: 16 /849,889 a therapeutic modality and provide a method of treating cancer, immunological disorders and other disease . ( 22 ) Filed : Apr. 15 , 2020 Specification includes a Sequence Listing . Matripase ST 14 Cleaves an IFN Mask from the Heavy Chain of an anti CD138 Fusion Ab . 1 2 3 1. ant - CD138 / Na 2. anti - C0138 IFNa mask 3. anti - C0138 FNa mask w / MST14 Patent Application Publication Oct. -
United States Patent (10) Patent No.: US 9,464,124 B2 Bancel Et Al
USOO9464124B2 (12) United States Patent (10) Patent No.: US 9,464,124 B2 Bancel et al. (45) Date of Patent: Oct. 11, 2016 (54) ENGINEERED NUCLEIC ACIDS AND 4,500,707 A 2f1985 Caruthers et al. METHODS OF USE THEREOF 4,579,849 A 4, 1986 MacCoSS et al. 4,588,585 A 5/1986 Mark et al. 4,668,777 A 5, 1987 Caruthers et al. (71) Applicant: Moderna Therapeutics, Inc., 4,737.462 A 4, 1988 Mark et al. Cambridge, MA (US) 4,816,567 A 3/1989 Cabilly et al. 4,879, 111 A 11/1989 Chong (72) Inventors: Stephane Bancel, Cambridge, MA 4,957,735 A 9/1990 Huang (US); Jason P. Schrum, Philadelphia, 4.959,314 A 9, 1990 Mark et al. 4,973,679 A 11/1990 Caruthers et al. PA (US); Alexander Aristarkhov, 5.012.818 A 5/1991 Joishy Chestnut Hill, MA (US) 5,017,691 A 5/1991 Lee et al. 5,021,335 A 6, 1991 Tecott et al. (73) Assignee: Moderna Therapeutics, Inc., 5,036,006 A 7, 1991 Sanford et al. Cambridge, MA (US) 9. A 228 at al. J. J. W. OS a 5,130,238 A 7, 1992 Malek et al. (*) Notice: Subject to any disclaimer, the term of this 5,132,418 A 7, 1992 °N, al. patent is extended or adjusted under 35 5,153,319 A 10, 1992 Caruthers et al. U.S.C. 154(b) by 0 days. 5,168,038 A 12/1992 Tecott et al. 5,169,766 A 12/1992 Schuster et al. -
Macrophage Activation: Dissociation of Cytotoxic Activity from Ia-A Antigen Expression (Fibroblast Interferon/Immune Interferon/Lymphokine) ELLIOTT J
Proc. Nati. Acad. Sci. USA Vol. 80, pp. 2031-2035, April 1983 Immunology Macrophage activation: Dissociation of cytotoxic activity from Ia-A antigen expression (fibroblast interferon/immune interferon/lymphokine) ELLIOTT J. BLUMENTHAL, WALDEN K. ROBERTS, ADRIANA VASIL, AND DAVID W. TALMAGE Department of Microbiology and Immunology, University of Colorado Health Sciences Center, Denver, Colorado 80262 Contributed by David W. Talmage, December 20, 1982 ABSTRACT Peritoneal macrophages were obtained from MATERIALS AND METHODS DBA/2 mice that were untreated or after the injection of bacillus Cainette-Guerin (BCG), thioglycollate broth, proteose-peptone Mice. Our source of peritoneal macrophages was DBA/2 broth, or gamma-irradiated P-815 tumor cells. These macro- mice that were less than 3 months old (The Jackson Labo- phages were "activated" to become cytotoxic for a fibroblast cell ratory). line (L 929) by the addition of lymphokines (LKs), lipopolysac- Elicitation of Peritoneal Macrophages. Peritoneal exudate charide (LPS), or fibroblast interferon (IFN-.3), and the expres- cells were collected by lavage with 5 ml of sterile Eagle min- sion of I region-associated antigens (Ia-Ad) on the macrophages imal essential medium. Resident cells were removed from un- was examined both before and after activation. Thioglycollate- treated mice. Cells were also obtained (a) 3-4 days after the elicited macrophages became Ia-A' when activated by LKs, but injection of 1 ml of 3% thioglycollate in broth that had been they remained la-A- when activated by LPS or IFN-f3. Resident "aged" for at least 6 months at 40C or (b) 3 days after intra- macrophages and proteose-peptone-elicited macrophages re- peritoneal injection of 1 ml of 1% proteose-peptone broth. -
A Role for Stat-1 in Regulating Interleukin 10 Production Following Lps Challenge
A ROLE FOR STAT-1 IN REGULATING INTERLEUKIN 10 PRODUCTION FOLLOWING LPS CHALLENGE DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University by Jeffrey Bryan VanDeusen, B.A. * * * * * The Ohio State University 2004 Dissertation Committee: Approved by Clay Marsh, MD Christoph Plass, PhD _______________________________ Michael A. Caligiuri, MD Denis Guttridge, PhD Adviser Department of Molecular Virology, Immunology, and Molecular Genetics ABSTRACT There have been substantial advances in understanding the events that regulate gene expression at the cellular and molecular level, however, there has been limited progress integrating this information to understand how biological systems function in vivo. Complementary DNA and protein microarray technologies in combination with sophisticated bioinformatics may eventually provide important insight into how biologic systems work in vivo. We hypothesized that assessments of such events in vivo would provide new insights into the immune response that could not be predicted or discovered ex vivo. Here, we describe the use of quantitative real time RT-PCR to serially quantify expression of a variety of pro- and anti-inflammatory cytokine genes in a number of individual tissues before, during, and after challenge with lipopolysaccharide (LPS). The data provide new insight into the heterogeneity of cytokine gene expression from organ to organ following infectious insult in vivo, as well as a greater understanding of cytokine regulation. For example, the anti- inflammatory cytokine interleukin-10 (IL-10) is thought to down-regulate the effects of the pro-inflammatory cytokine interferon gamma (IFN-γ) on monocyte activation following lipopolysaccharide (LPS) stimulation. -
W O 2014/151535 a L 2 5 September 2014 (25.09.2014) 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 W O 2014/151535 A l 2 5 September 2014 (25.09.2014) P O P C T (51) International Patent Classification: HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, C07K 14/705 (2006.01) KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, (21) International Application Number: OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, PCT/US20 14/025940 SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, (22) International Filing Date: TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, 13 March 2014 (13.03.2014) ZW. (25) Filing Language: English (84) Designated States (unless otherwise indicated, for every kind of regional protection available): ARIPO (BW, GH, (26) Publication Language: English GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, SZ, TZ, (30) Priority Data: UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, TJ, 61/791,537 15 March 2013 (15.03.2013) TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, 61/787,753 15 March 2013 (15.03.2013) EE, ES, FI, FR, GB, GR, HR, HU, IE, IS, IT, LT, LU, LV, MC, MK, MT, NL, NO, PL, PT, RO, RS, SE, SI, SK, SM, (71) Applicant: BAYER HEALTHCARE LLC [US/US]; 555 TR), OAPI (BF, BJ, CF, CG, CI, CM, GA, GN, GQ, GW, White Plains Rd., Tarrytown, NY 10591 (US). -
Long Non-Coding RNA GRASLND Enhances Chondrogenesis Via Suppression of Interferon 4 Type II Signaling Pathway 5 Authors: Nguyen P.T
bioRxiv preprint doi: https://doi.org/10.1101/650010; this version posted May 24, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Classification: Biological Sciences with a minor category of Cell Biology 2 3 Title: Long non-coding RNA GRASLND enhances chondrogenesis via suppression of interferon 4 type II signaling pathway 5 Authors: Nguyen P.T. Huynha,b,c,d, Catherine C. Glossa,b,d, Jeremiah Lorentza,b,d, Ruhang 6 Tanga,b,d, Jonathan M. Brungere, Audrey McAlindena,b,d, Bo Zhangd, Farshid GuilaKa,b,d 7 8 Short title: LncRNA GRASLND suppresses IFN to enhance chondrogenesis 9 10 Author Affiliation: 11 a. Department of Orthopaedic Surgery, Washington University in St Louis, MO, USA, 63110 12 b. Shriners Hospitals for Children – St. Louis, St. Louis, MO, USA, 63110 13 c. Department of Cell Biology, Duke University, NC, USA, 27708 14 d. Center of Regenerative Medicine, Washington University in St Louis, MO, USA, 63110 15 e. Department of Cellular and Molecular Pharmacology, University of California, San Francisco, 16 CA, USA, 94158 17 18 19 Corresponding Author: 20 Farshid Guilak 21 Campus Box 8233 22 McKinley Research Building, Room 3121 23 St Louis, MO, USA, 63110 24 Email Address: [email protected] 25 26 Keywords: mesenchymal stem cells, tissue engineering, regenerative medicine, 27 RNF144A-AS1 28 1 bioRxiv preprint doi: https://doi.org/10.1101/650010; this version posted May 24, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. -
Severe Sepsis Epidemiology and Sex-Related Differences in Inflammatory Markers
UMEÅ UNIVERSITY MEDICAL DISSERTATIONS NEW SERIES NO. 1680 ISSN 0346-6612 ISBN: 978-91-7601-149-2 From the Department of Surgical and Perioperative Sciences Anesthesiology and Intensive Care Medicine Umeå University, Sweden Severe sepsis Epidemiology and sex-related differences in inflammatory markers. Sofie Jacobson Fakultetsopponent: Professor Else Tönnesen Dept. of Clinical Medicine - Anaesthesiology Århus, Danmark Umeå 2014 Cover illustration: "First line of defence" Anders Jacobsson Copyright © 2014 Sofie Jacobson ISBN: 978-91-7601-149-2 NEW SERIES NO. 1680 ISSN 0346-6612 Layout and printed by: Print & Media Umeå, Sweden 2014 To my family A goal is a dream with a deadline. ~ Napolean Hill Contents CONTENTS ABSTRACT......................................................................................................................... iv Svensk sammanfattning .........................................................................................................v Abbreviations..................................................................................................................... viii ORIGINAL PAPERS............................................................................................................x PROLOGUE ........................................................................................................................xi INTRODUCTION..................................................................................................................1 Epidemiology ....................................................................................................................2 -
The Role of Interferons in the Pathogenesis of Sjögren's Syndrome and Future Therapeutic Perspectives
biomolecules Review The Role of Interferons in the Pathogenesis of Sjögren’s Syndrome and Future Therapeutic Perspectives Nicoletta Del Papa 1,* , Antonina Minniti 1, Maurizio Lorini 2, Vincenzo Carbonelli 2, Wanda Maglione 1, Francesca Pignataro 1, Nicola Montano 2 , Roberto Caporali 1,3 and Claudio Vitali 4 1 Department of Rheumatology, ASST G. Pini-CTO, 20122 Milano, Italy; [email protected] (A.M.); [email protected] (W.M.); [email protected] (F.P.); [email protected] (R.C.) 2 Department of Clinical Sciences and Community Health, Ca’ Granda IRCCS Foundation, Ospedale Maggiore Policlinico, Università degli Studi di Milano, 20122 Milano, Italy; [email protected] (M.L.); [email protected] (V.C.); [email protected] (N.M.) 3 Research Center for Adult and Pediatric Rheumatic Diseases, Department of Clinical Sciences and Community Health, Università degli Studi di Milano, 20122 Milano, Italy 4 Mater Domini Humanitas Hospital, Rheumatology Outpatient Clinics, 21053 Castellanza, Italy; [email protected] * Correspondence: [email protected] Abstract: There is a great deal of evidence pointing to interferons (IFNs) as being key cytokines in the pathogenesis of different systemic autoimmune diseases, including primary Sjögren’s syndrome (pSS). In this disease, a large number of studies have shown that an overexpression of type I IFN, the ‘so-called’ type I IFN signature, is present in peripheral blood mononuclear cells, and that this finding is associated with the development of systemic extra-glandular manifestations, and a Citation: Del Papa, N.; Minniti, A.; substantial production of autoantibodies and inflammatory cytokines. -
Immunosenescence and Exercise-Mediated Modulation of the Innate Immune Response to Influenza Infection in Mice Shibani Naik Iowa State University
Iowa State University Capstones, Theses and Graduate Theses and Dissertations Dissertations 2013 Immunosenescence and exercise-mediated modulation of the innate immune response to Influenza infection in mice Shibani Naik Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/etd Part of the Allergy and Immunology Commons, Family, Life Course, and Society Commons, Immunology and Infectious Disease Commons, Medical Immunology Commons, and the Physical Therapy Commons Recommended Citation Naik, Shibani, "Immunosenescence and exercise-mediated modulation of the innate immune response to Influenza infection in mice" (2013). Graduate Theses and Dissertations. 13342. https://lib.dr.iastate.edu/etd/13342 This Dissertation is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Graduate Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. Immunosenescence and exercise-mediated modulation of the innate immune response to Influenza infection in mice by Shibani Naik A dissertation submitted to the graduate faculty in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY Major: Immunobiology Program of Study Committee: Marian Kohut, Major Professor Mark Ackermann Joan Cunnick Peter Nara Daniel Nettleton Iowa State University Ames, Iowa 2013 Copyright © Shibani Naik, 2013. All rights reserved. ii TABLE OF CONTENTS ABSTRACT iv CHAPTER 1. GENERAL INTRODUCTION Introduction to the Dissertation 01 Literature Review: Influenza viral infection 01 Immune response to influenza infection 08 Immunosenescence 25 Exercise and the Immune System 37 CHAPTER 2.