RT² Profiler PCR Array (384-Well Format) Human Inflammatory Response & Autoimmunity
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C19) United States C12) Patent Application Publication C10) Pub
1111111111111111 IIIIII IIIII 1111111111 11111 11111 111111111111111 1111111111 1111111111 11111111 US 20200081016Al c19) United States c12) Patent Application Publication c10) Pub. No.: US 2020/0081016 Al Talaat et al. (43) Pub. Date: Mar. 12, 2020 (54) BIOMARKERS FOR EARLY DIAGNOSIS Publication Classification AND DIFFERENTIATION OF (51) Int. Cl. MYCOBACTERIAL INFECTION GOIN 33/68 (2006.01) C12Q 116851 (2006.01) (71) Applicant: Wisconsin Alumni Research GOIN 33/569 (2006.01) Foundation, Madison, WI (US) (52) U.S. Cl. (72) Inventors: Adel Mohamed Talaat, Madison, WI CPC ......... GOIN 33/6854 (2013.01); GOIN 33/68 (US); Chia-wei Wu, Madison, WI (US) (2013.01); GOIN 2800/50 (2013.01); GOIN 33/5695 (2013.01); GOIN 2800/26 (2013.01); (21) Appl. No.: 16/555,819 C12Q 116851 (2013.01) (22) Filed: Aug. 29, 2019 (57) ABSTRACT Mycobacterial-specific biomarkers and methods of using Related U.S. Application Data such biomarkers for diagnosis of mycobacterial infection in (60) Provisional application No. 62/728,387, filed on Sep. a mammal are disclosed. 7, 2018. Specification includes a Sequence Listing. Patent Application Publication Mar. 12, 2020 Sheet 1 of 10 US 2020/0081016 Al FIG. 1 ·~{:: -{t i * !lpNbiNi$ 1 !lpN p~ra 111:111111 llillllll: 111!11,111llltllllll~ 11111 ■111 ~; C,,Nmnsus KR.IGINMTKX L.lC(X.AXXXXG AXXXXMPXTX RXO-GXVXXVG VKVXPWIPTX ® • ® l I I iipN lK>V(S ~Hl!lli!Wiofflij 1!11.llofJiillj mllB~lijftlt flol=fiolill ••t-il-~MM ~9 llpN p~ra HfHJoffit:torti ilffllGNillm miJllt~ttiollf ~•01:101111 llm:l:l1IA@~ iOO C,,nstmsus XXRXLXXGRS Vt IOGNT.LDP i LOt.MLSXXR XXGXOG.I...XVO ODXXXSR:AXM t2:;: i-/4~~ ! l 1 I~~~~b;:: llllil~l:1:1 llil 111111:1~:111~ 1111111::;1 1lllilllll: ~:~ C,,nimnsus XXXXXXXPGP QtHVDVXXI...X XPGPAGXIPA RHYRPXGGXX QXPt.l...VFYHG Consl:lrvat,ofl -:§;::. -
Early Detection of Peripheral Blood Cell Signature in Children Developing B-Cell Autoimmunity at a Young Age
2024 Diabetes Volume 68, October 2019 Early Detection of Peripheral Blood Cell Signature in Children Developing b-Cell Autoimmunity at a Young Age Henna Kallionpää,1 Juhi Somani,2 Soile Tuomela,1 Ubaid Ullah,1 Rafael de Albuquerque,1 Tapio Lönnberg,1 Elina Komsi,1 Heli Siljander,3,4 Jarno Honkanen,3,4 Taina Härkönen,3,4 Aleksandr Peet,5,6 Vallo Tillmann,5,6 Vikash Chandra,3,7 Mahesh Kumar Anagandula,8 Gun Frisk,8 Timo Otonkoski,3,7 Omid Rasool,1 Riikka Lund,1 Harri Lähdesmäki,2 Mikael Knip,3,4,9,10 and Riitta Lahesmaa1 Diabetes 2019;68:2024–2034 | https://doi.org/10.2337/db19-0287 The appearance of type 1 diabetes (T1D)-associated function before T1D and suggest a potential role for IL32 autoantibodies is the first and only measurable param- in the pathogenesis of T1D. eter to predict progression toward T1D in genetically susceptible individuals. However, autoantibodies indi- cate an active autoimmune reaction, wherein the im- Family and sibling studies in type 1 diabetes (T1D) have mune tolerance is already broken. Therefore, there is implicated a firm genetic predisposition to a locus con- a clear and urgent need for new biomarkers that predict taining HLA class I and class II genes on chromosome the onset of the autoimmune reaction preceding auto- 6 suggesting a role for CD4+ as well as CD8+ T cells in T1D fl antibody positivity or re ect progressive b-cell destruc- pathogenesis (1–3). As much as 30–50% of the genetic risk – tion. Here we report the mRNA sequencing based is conferred by HLA class II molecules, which are crucial in analysis of 306 samples including fractionated samples antigen presentation to CD4+ T cells. -
T CELLS a Killer Cytokine
RESEARCH HIGHLIGHTS S.Bradbrook/NPG T CELLS A killer cytokine T helper 17 (TH17) cells have specific for IL-26 or small interfering with live human cells. However, well-known antimicrobial and RNA against IL26. Similar to other when IL-26 was mixed with irradi- inflammatory functions, but exactly cationic antimicrobial peptides, such ated human cells to trigger cell how these functions are mediated as LL-37 and human β-defensin 3, death, IFNα production by pDCs is unclear. New research shows recombinant IL-26 was shown to was induced, and this was largely that the human TH17 cell-derived disrupt bacterial membranes by abrogated by DNase treatment. cytokine interleukin-26 (IL-26) pore formation. To investigate the mechanism of functions like an antimicrobial As LL-37 has been shown to form IFNα induction, the authors used peptide, directly lysing bacteria and complexes with extracellular DNA, fluorochrome-labelled DNA to track promoting immunogenicity of DNA the authors next tested whether this IL-26–DNA complexes in pDCs. from dead bacteria and host cells. was also the case for IL-26. Indeed, They found that the complexes were Three-dimensional modelling when mixed with bacterial DNA, internalized by pDCs through endo- of IL-26 showed that its structure is IL-26 formed insoluble particles cytosis following attachment to mem- unlike that of other cytokines from with DNA. Moreover, compared brane heparin-sulfate proteoglycans. the same family, and instead it shares with IL-26 alone or bacterial Once inside the cell, the IL-26–DNA features with antimicrobial peptides: DNA alone, IL-26–DNA com- complexes activated endosomal specifically, an amphipathic structure, plexes induced the production of Toll-like receptor 9 (TLR9), which with clusters of cationic charges, and interferon-α (IFNα) by plasmacytoid promotes IFNα production. -
Interleukin-10 Family and Tuberculosis: an Old Story Renewed Abualgasim Elgaili Abdalla1, 2, Nzungize Lambert1, Xiangke Duan1, Jianping Xie1
Int. J. Biol. Sci. 2016, Vol. 12 710 Ivyspring International Publisher International Journal of Biological Sciences 2016; 12(6): 710-717. doi: 10.7150/ijbs.13881 Review Interleukin-10 Family and Tuberculosis: An Old Story Renewed Abualgasim Elgaili Abdalla1, 2, Nzungize Lambert1, Xiangke Duan1, Jianping Xie1 1. Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, Key Laboratory of Eco-environments in Three Gorges Reservoir Region, Ministry of Education, School of Life Sciences, Southwest University, Beibei, Chongqing 400715, China. 2. Department of Clinical Microbiology, College of Medical Laboratory Sciences, Omdurman Islamic University, Omdurman, Khartoum, Sudan. Corresponding author: Jianping Xie E-mail: [email protected] Tel&Fax: 862368367108. © Ivyspring International Publisher. Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. See http://ivyspring.com/terms for terms and conditions. Received: 2015.09.17; Accepted: 2016.01.15; Published: 2016.04.27 Abstract The interleukin-10 (IL-10) family of cytokines consists of six immune mediators, namely IL-10, IL-19, IL-20, IL-22, IL-24 and IL-26. IL-10, IL-22, IL-24 and IL-26 are critical for the regulation of host defense against Mycobacterium tuberculosis infections. Specifically, IL-10 and IL-26 can suppress the antimycobacterial immunity and promote the survival of pathogen, while IL-22 and IL-24 can generate protective responses and inhibit the intracellular growth of pathogen. Knowledge about the new players in tuberculosis immunology, namely IL-10 family, can inform novel immunity-based countermeasures and host directed therapies against tuberculosis. -
Interleukin 28 Is a Potential Therapeutic Target for Sepsis
Clinical Immunology 205 (2019) 29–34 Contents lists available at ScienceDirect Clinical Immunology journal homepage: www.elsevier.com/locate/yclim Interleukin 28 is a potential therapeutic target for sepsis T ⁎ Qin Luoa,b, Yi Liuc, Shuang Liub, Yibing Yinb, Banglao Xud, Ju Caoa, a Department of Laboratory Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China b Key Laboratory of Diagnostic Medicine designated by the Ministry of Education, Chongqing Medical University, Chongqing, China c Department of Intensive Care Unit, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China d Department of Laboratory Medicine, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China ARTICLE INFO ABSTRACT Keywords: Identification of new therapeutic targets for the treatment of sepsis is imperative. We report here that cytokine Interleukin-28 IL-28 (IFN-λ) levels were elevated in clinical and experimental sepsis. Neutralization of IL-28 protected mice Sepsis from lethal sepsis induced by cecal ligation and puncture (CLP), which was associated with improved bacterial Infection clearance and enhanced neutrophil infiltration. Conversely, administration of recombinant IL-28 aggravated Immunity mortality, facilitated bacterial dissimilation and limited neutrophil recruitment, in the model of sepsis induced Neutrophil by CLP. This study defines IL-28 as a detrimental mediator during sepsis and identifies a potential therapeutic target for the immune therapy in sepsis. 1. Introduction immunopathology of sepsis is still poorly understood. To address this issue, we examined the potential role of IL-28 in the Each year, about 31.5 million individuals develop sepsis, and up to progression of sepsis. -
Cytokine Nomenclature
RayBiotech, Inc. The protein array pioneer company Cytokine Nomenclature Cytokine Name Official Full Name Genbank Related Names Symbol 4-1BB TNFRSF Tumor necrosis factor NP_001552 CD137, ILA, 4-1BB ligand receptor 9 receptor superfamily .2. member 9 6Ckine CCL21 6-Cysteine Chemokine NM_002989 Small-inducible cytokine A21, Beta chemokine exodus-2, Secondary lymphoid-tissue chemokine, SLC, SCYA21 ACE ACE Angiotensin-converting NP_000780 CD143, DCP, DCP1 enzyme .1. NP_690043 .1. ACE-2 ACE2 Angiotensin-converting NP_068576 ACE-related carboxypeptidase, enzyme 2 .1 Angiotensin-converting enzyme homolog ACTH ACTH Adrenocorticotropic NP_000930 POMC, Pro-opiomelanocortin, hormone .1. Corticotropin-lipotropin, NPP, NP_001030 Melanotropin gamma, Gamma- 333.1 MSH, Potential peptide, Corticotropin, Melanotropin alpha, Alpha-MSH, Corticotropin-like intermediary peptide, CLIP, Lipotropin beta, Beta-LPH, Lipotropin gamma, Gamma-LPH, Melanotropin beta, Beta-MSH, Beta-endorphin, Met-enkephalin ACTHR ACTHR Adrenocorticotropic NP_000520 Melanocortin receptor 2, MC2-R hormone receptor .1 Activin A INHBA Activin A NM_002192 Activin beta-A chain, Erythroid differentiation protein, EDF, INHBA Activin B INHBB Activin B NM_002193 Inhibin beta B chain, Activin beta-B chain Activin C INHBC Activin C NM005538 Inhibin, beta C Activin RIA ACVR1 Activin receptor type-1 NM_001105 Activin receptor type I, ACTR-I, Serine/threonine-protein kinase receptor R1, SKR1, Activin receptor-like kinase 2, ALK-2, TGF-B superfamily receptor type I, TSR-I, ACVRLK2 Activin RIB ACVR1B -
Cytokines and Their Genetic Polymorphisms Related to Periodontal Disease
Journal of Clinical Medicine Review Cytokines and Their Genetic Polymorphisms Related to Periodontal Disease Małgorzata Kozak 1, Ewa Dabrowska-Zamojcin 2, Małgorzata Mazurek-Mochol 3 and Andrzej Pawlik 4,* 1 Chair and Department of Dental Prosthetics, Pomeranian Medical University, Powsta´nców Wlkp 72, 70-111 Szczecin, Poland; [email protected] 2 Department of Pharmacology, Pomeranian Medical University, Powsta´nców Wlkp 72, 70-111 Szczecin, Poland; [email protected] 3 Department of Periodontology, Pomeranian Medical University, Powsta´nców Wlkp 72, 70-111 Szczecin, Poland; [email protected] 4 Department of Physiology, Pomeranian Medical University, Powsta´nców Wlkp 72, 70-111 Szczecin, Poland * Correspondence: [email protected] Received: 24 October 2020; Accepted: 10 December 2020; Published: 14 December 2020 Abstract: Periodontal disease (PD) is a chronic inflammatory disease caused by the accumulation of bacterial plaque biofilm on the teeth and the host immune responses. PD pathogenesis is complex and includes genetic, environmental, and autoimmune factors. Numerous studies have suggested that the connection of genetic and environmental factors induces the disease process leading to a response by both T cells and B cells and the increased synthesis of pro-inflammatory mediators such as cytokines. Many studies have shown that pro-inflammatory cytokines play a significant role in the pathogenesis of PD. The studies have also indicated that single nucleotide polymorphisms (SNPs) in cytokine genes may be associated with risk and severity of PD. In this narrative review, we discuss the role of selected cytokines and their gene polymorphisms in the pathogenesis of periodontal disease. Keywords: periodontal disease; cytokines; polymorphism 1. -
Overlapping, Additive and Counterregulatory Effects of Type II and I Interferons on Myeloid Dendritic Cell Functions
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Serveur académique lausannois Review Article TheScientificWorldJOURNAL (2011) 11, 2071–2090 ISSN 1537-744X; doi:10.1100/2011/873895 Overlapping, Additive and Counterregulatory Effects of Type II and I Interferons on Myeloid Dendritic Cell Functions Loredana Frasca and Roberto Lande Department of Infectious, Parasitic and Immune-mediated Diseases, Istituto Superiore di Sanita,` 00161 Rome, Italy Received 8 April 2011; Accepted 27 September 2011 Academic Editor: Fulvio D’Acquisto Dendritic cells (DCs) are central player in immunity by bridging the innate and adaptive arms of the immune system (IS). Interferons (IFNs) are one of the most important factors that regulate both innate and adaptive immunity too. Thus, the understanding of how type II and I IFNs modulate the immune-regulatory properties of DCs is a central issue in immunology. In this paper, we will address this point in the light of the most recent literature, also highlighting the controversial data reported in the field. According to the wide literature available, type II as well as type I IFNs appear, at the same time, to collaborate, to induce additive effects or overlapping functions, as well as to counterregulate each one’s effects on DC biology and, in general, the immune response. The knowledge of these effects has important therapeutic implications in the treatment of infec- tious/autoimmune diseases and cancer and indicates strategies for using IFNs as vaccine adju- vants and in DC-based immune therapeutic approaches. KEYWORDS: IFNs, dendritic cell effector functions, immune activation, immune regulation, cross- regulation Correspondence should be addressed to Loredana Frasca, [email protected] Copyright © 2011 L. -
Therapeutic and Prophylactic Use of Oral, Low-Dose Ifns in Species of Veterinary Interest: Back to the Future
veterinary sciences Review Therapeutic and Prophylactic Use of Oral, Low-Dose IFNs in Species of Veterinary Interest: Back to the Future Sara Frazzini 1 , Federica Riva 2,* and Massimo Amadori 3 1 Gastroenterology and Endoscopy Unit, Fondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico, 20122 Milan, Italy; [email protected] 2 Dipartimento di Medicina Veterinaria, Università degli Studi di Milano, 26900 Lodi, Italy 3 Rete Nazionale di Immunologia Veterinaria, 25125 Brescia, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-0250334519 Abstract: Cytokines are important molecules that orchestrate the immune response. Given their role, cytokines have been explored as drugs in immunotherapy in the fight against different pathological conditions such as bacterial and viral infections, autoimmune diseases, transplantation and cancer. One of the problems related to their administration consists in the definition of the correct dose to avoid severe side effects. In the 70s and 80s different studies demonstrated the efficacy of cytokines in veterinary medicine, but soon the investigations were abandoned in favor of more profitable drugs such as antibiotics. Recently, the World Health Organization has deeply discouraged the use of antibiotics in order to reduce the spread of multi-drug resistant microorganisms. In this respect, the use of cytokines to prevent or ameliorate infectious diseases has been highlighted, and several studies show the potential of their use in therapy and prophylaxis also in the veterinary field. In this review we aim to review the principles of cytokine treatments, mainly IFNs, and to update the experiences encountered in animals. Keywords: veterinary immunotherapy; cytokines; IFN; low dose treatment; oral treatment Citation: Frazzini, S.; Riva, F.; Amadori, M. -
Mechanism of Action Through an IFN Type I-Independent Responses To
Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 is online at: average * The Journal of Immunology , 12 of which you can access for free at: 2012; 188:3088-3098; Prepublished online 20 from submission to initial decision 4 weeks from acceptance to publication February 2012; doi: 10.4049/jimmunol.1101764 http://www.jimmunol.org/content/188/7/3088 MF59 and Pam3CSK4 Boost Adaptive Responses to Influenza Subunit Vaccine through an IFN Type I-Independent Mechanism of Action Elena Caproni, Elaine Tritto, Mario Cortese, Alessandro Muzzi, Flaviana Mosca, Elisabetta Monaci, Barbara Baudner, Anja Seubert and Ennio De Gregorio J Immunol cites 33 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription http://www.jimmunol.org/content/suppl/2012/02/21/jimmunol.110176 4.DC1 This article http://www.jimmunol.org/content/188/7/3088.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2012 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 -
United States Patent (19) 11 Patent Number: 5,766,866 Center Et Al
USOO5766866A United States Patent (19) 11 Patent Number: 5,766,866 Center et al. 45) Date of Patent: Jun. 16, 1998 54 LYMPHOCYTE CHEMOATTRACTANT Center, et al. The Journal of Immunology. 128:2563-2568 FACTOR AND USES THEREOF (1982). 75 Inventors: David M. Center. Wellesley Hills; Cruikshank, et al. The Journal of Immunology, William W. Cruikshank. Westford; 138:3817-3823 (1987). Hardy Kornfeld, Brighton, all of Mass. Cruikshank, et al., The Journal of Immunology, 73) Assignee: Research Corporation Technologies, 146:2928-2934 (1991). Inc., Tucson, Ariz. Cruikshank, et al., EMBL Database. Accession No. M90301 (21) Appl. No.: 580,680 (1992). 22 Filed: Dec. 29, 1995 Cruikshank. et al. The Journal of Immunology, 128:2569-2574 (1982). Related U.S. Application Data Rand, et al., J. Exp. Med., 173:1521-1528 (1991). 60 Division of Ser. No. 480,156, Jun. 7, 1995, which is a continuation-in-part of Ser. No. 354,961, Dec. 13, 1994, Harlow (1988) Antibodies, a laboratory manual. Cold Spring which is a continuation of Ser. No. 68,949, May 21, 1993, Harbor Laboratory, 285, 287. abandoned. Waldman (1991) Science. vol. 252, 1657-1662. (51) Int. Cl. ....................... G01N 33/53; CO7K 1700; CO7K 16/00: A61K 45/05 Hams et al. (1993) TIBTECH Feb. 1993 vol. 111, 42-44. 52 U.S. Cl. ......................... 424/7.24; 435/7.1; 435/7.92: 435/975; 530/350:530/351; 530/387.1: Center, et al. (Feb. 1995) "The Lymphocyte Chemoattractant 530/388.23: 530/389.2: 424/85.1: 424/130.1 Factor”. J. Lab. Clin. Med. 125(2):167-172. -
Interleukin-21 Is Required for the Development of Type 1 Diabetes in NOD Mice Andrew P.R
ORIGINAL ARTICLE Interleukin-21 Is Required for the Development of Type 1 Diabetes in NOD Mice Andrew P.R. Sutherland,1,2 Tom Van Belle,3 Andrea L. Wurster,1 Akira Suto,1 Monia Michaud,1 Dorothy Zhang,1 Michael J. Grusby,1,4 and Matthias von Herrath3 OBJECTIVE—Interleukin (IL)-21 is a type 1 cytokine that has known as insulin-dependent diabetes (idd) loci that confer been implicated in the pathogenesis of type 1 diabetes via the susceptibility to or protection from the development of unique biology of the nonobese diabetic (NOD) mouse strain. type 1 diabetes (2). Of the ϳ15 regions identified, idd3isof The aim of this study was to investigate a causal role for IL-21 in particular importance, because congenic NOD lines con- type 1 diabetes. taining alleles from protected strains at this locus are RESEARCH DESIGN AND METHODS—We generated IL- significantly less susceptible to diabetes. To date, idd3is 21R–deficient NOD mice and C57Bl/6 mice expressing IL-21 in the most potent disease modifying the non–major histo- pancreatic -cells, allowing the determination of the role of compatibility complex (MHC) locus (3). Therefore, some insufficient and excessive IL-21 signaling in type 1 diabetes. of the genes within the idd3 interval must play a crucial role in regulating immune destruction of pancreatic RESULTS—Deficiency in IL-21R expression renders NOD mice  resistant to insulitis, production of insulin autoantibodies, and -cells. onset of type 1 diabetes. The lymphoid compartment in IL- Among the several candidate genes within the idd3 21RϪ/Ϫ NOD is normal and does not contain an increased locus, interleukin (IL)-21 is of particular interest, because regulatory T-cell fraction or diminished effector cytokine re- dysregulated IL-21 production and signaling has been sponses.