Recombinant Human Cytokines
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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. -
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 -
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. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Protein Identities in Evs Isolated from U87-MG GBM Cells As Determined by NG LC-MS/MS
Protein identities in EVs isolated from U87-MG GBM cells as determined by NG LC-MS/MS. No. Accession Description Σ Coverage Σ# Proteins Σ# Unique Peptides Σ# Peptides Σ# PSMs # AAs MW [kDa] calc. pI 1 A8MS94 Putative golgin subfamily A member 2-like protein 5 OS=Homo sapiens PE=5 SV=2 - [GG2L5_HUMAN] 100 1 1 7 88 110 12,03704523 5,681152344 2 P60660 Myosin light polypeptide 6 OS=Homo sapiens GN=MYL6 PE=1 SV=2 - [MYL6_HUMAN] 100 3 5 17 173 151 16,91913397 4,652832031 3 Q6ZYL4 General transcription factor IIH subunit 5 OS=Homo sapiens GN=GTF2H5 PE=1 SV=1 - [TF2H5_HUMAN] 98,59 1 1 4 13 71 8,048185945 4,652832031 4 P60709 Actin, cytoplasmic 1 OS=Homo sapiens GN=ACTB PE=1 SV=1 - [ACTB_HUMAN] 97,6 5 5 35 917 375 41,70973209 5,478027344 5 P13489 Ribonuclease inhibitor OS=Homo sapiens GN=RNH1 PE=1 SV=2 - [RINI_HUMAN] 96,75 1 12 37 173 461 49,94108966 4,817871094 6 P09382 Galectin-1 OS=Homo sapiens GN=LGALS1 PE=1 SV=2 - [LEG1_HUMAN] 96,3 1 7 14 283 135 14,70620005 5,503417969 7 P60174 Triosephosphate isomerase OS=Homo sapiens GN=TPI1 PE=1 SV=3 - [TPIS_HUMAN] 95,1 3 16 25 375 286 30,77169764 5,922363281 8 P04406 Glyceraldehyde-3-phosphate dehydrogenase OS=Homo sapiens GN=GAPDH PE=1 SV=3 - [G3P_HUMAN] 94,63 2 13 31 509 335 36,03039959 8,455566406 9 Q15185 Prostaglandin E synthase 3 OS=Homo sapiens GN=PTGES3 PE=1 SV=1 - [TEBP_HUMAN] 93,13 1 5 12 74 160 18,68541938 4,538574219 10 P09417 Dihydropteridine reductase OS=Homo sapiens GN=QDPR PE=1 SV=2 - [DHPR_HUMAN] 93,03 1 1 17 69 244 25,77302971 7,371582031 11 P01911 HLA class II histocompatibility antigen, -
Cyclooxygenase-2 Inflammatory Factors, IL-29, IL-8, And
Hepatitis B Virus Induces a Novel Inflammation Network Involving Three Inflammatory Factors, IL-29, IL-8, and Cyclooxygenase-2 This information is current as of September 27, 2021. Yi Yu, Rui Gong, Yongxin Mu, Yanni Chen, Chengliang Zhu, Zhichen Sun, Mingzhou Chen, Yingle Liu, Ying Zhu and Jianguo Wu J Immunol 2011; 187:4844-4860; Prepublished online 28 September 2011; Downloaded from doi: 10.4049/jimmunol.1100998 http://www.jimmunol.org/content/187/9/4844 http://www.jimmunol.org/ References This article cites 55 articles, 29 of which you can access for free at: http://www.jimmunol.org/content/187/9/4844.full#ref-list-1 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 27, 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 © 2011 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Hepatitis B Virus Induces a Novel Inflammation Network Involving Three Inflammatory Factors, IL-29, IL-8, and Cyclooxygenase-2 Yi Yu,*,†,‡ Rui Gong,*,† Yongxin Mu,*,† Yanni Chen,*,†,‡ Chengliang Zhu,*,† Zhichen Sun,*,† Mingzhou Chen,*,†,‡ Yingle Liu,*,†,‡ Ying Zhu,*,†,‡ and Jianguo Wu*,†,‡ Chronic inflammation induced by hepatitis B virus (HBV) is a major causative factor associated with the development of cirrhosis and hepatocellular carcinoma. -
Regulation of Osteoblast Differentiation by Cytokine Networks
International Journal of Molecular Sciences Review Regulation of Osteoblast Differentiation by Cytokine Networks Dulshara Sachini Amarasekara 1, Sumi Kim 2 and Jaerang Rho 2,* 1 Department of Zoology and Environment Sciences, Faculty of Science, University of Colombo, Colombo 00300, Sri Lanka; [email protected] 2 Department of Microbiology and Molecular Biology, Chungnam National University, Daejeon 34134, Korea; [email protected] * Correspondence: [email protected]; Tel.: +82-42-821-6420; Fax: +82-42-822-7367 Abstract: Osteoblasts, which are bone-forming cells, play pivotal roles in bone modeling and remod- eling. Osteoblast differentiation, also known as osteoblastogenesis, is orchestrated by transcription factors, such as runt-related transcription factor 1/2, osterix, activating transcription factor 4, special AT-rich sequence-binding protein 2 and activator protein-1. Osteoblastogenesis is regulated by a network of cytokines under physiological and pathophysiological conditions. Osteoblastogenic cytokines, such as interleukin-10 (IL-10), IL-11, IL-18, interferon-γ (IFN-γ), cardiotrophin-1 and oncostatin M, promote osteoblastogenesis, whereas anti-osteoblastogenic cytokines, such as tumor necrosis factor-α (TNF-α), TNF-β, IL-1α, IL-4, IL-7, IL-12, IL-13, IL-23, IFN-α, IFN-β, leukemia inhibitory factor, cardiotrophin-like cytokine, and ciliary neurotrophic factor, downregulate os- teoblastogenesis. Although there are gaps in the body of knowledge regarding the interplay of cytokine networks in osteoblastogenesis, cytokines appear to be potential therapeutic targets in bone- related diseases. Thus, in this study, we review and discuss our osteoblast, osteoblast differentiation, osteoblastogenesis, cytokines, signaling pathway of cytokine networks in osteoblastogenesis. Keywords: osteoblast; osteoblast differentiation; osteoblastogenesis; cytokine; signaling pathway Citation: Amarasekara, D.S.; Kim, S.; Rho, J. -
HUMAN INTERLEUKIN-29/INTERFERON-LAMBDA 1 Product Number: 11825-1 Lot Number: 5620 Expiration Date: October 2, 2013 Size: 25 Μg
HUMAN INTERLEUKIN-29/INTERFERON-LAMBDA 1 Product Number: 11825-1 Lot Number: 5620 Expiration Date: October 2, 2013 Size: 25 μg Description: Human Interleukin-29/Interferon-Lambda 1 Source: DNA sequence encoding the signal peptide from human CD33 was fused to the carboxyl terminally polyhistidine-tagged mature human IL-29 (Gly 20 - Thr 200) (Sheppard, P. et al., 2003, Nat. Immunol. 4(1):63 - 68). The chimeric protein was expressed in a mouse myeloma cell line, NS0. Form: Lyophilized Buffer: Phosphate-buffered saline (PBS) containing 50μg of bovine serum albumin (BSA) per 1 μg of cytokine Reconstitution: It is recommended that sterile PBS containing at least 0.1% human serum albumin or bovine serum albumin be added to the vial to prepare a stock solution of no less than 10μg/ml. Endotoxin: < 1 EU/μg Molecular Weight: Based on N-terminal sequencing, the mature recombinant IL-29 starts at Gly 20 and has a calculated molecular mass of 21.4 kDa. As a result of glycosylation, the recombinant monomer migrates as an approximately 26-35kDa protein in SDS-PAGE under reducing conditions. Purity: > 95% Synonyms: Hu IL-29; Hu IFN-λ1 Assays Used to Measure Bioactivity: Human HepG2 cells infected with encephalomyocarditis virus (Sheppard, P. et al., 2003, Nature Immunol. 4:63). The ED50 for this effect is typically 1- 5 ng/mL. Shipping Conditions: Wet Ice Physical State of Product During Shipping: Lyophilized Special Conditions/Comments: After receipt, this product should be kept at -70˚C or below for retention of full activity. Upon reconstitution, this cytokine can be stored under sterile conditions at -20˚C to -70˚C in a manual defrost freezer for three months without detection loss of activity. -
Secretome Screening Reveals Immunomodulating Functions Of
www.nature.com/scientificreports OPEN Secretome screening reveals immunomodulating functions of IFNα‑7, PAP and GDF‑7 on regulatory T‑cells Mei Ding1*, Rajneesh Malhotra2, Tomas Ottosson2, Magnus Lundqvist3, Aman Mebrahtu3, Johan Brengdahl1, Ulf Gehrmann2, Elisabeth Bäck4, Douglas Ross‑Thriepland5, Ida Isaksson6, Björn Magnusson1, Kris F. Sachsenmeier7, Hanna Tegel3, Sophia Hober3, Mathias Uhlén3, Lorenz M. Mayr5, Rick Davies5, Johan Rockberg3 & Lovisa Holmberg Schiavone1* Regulatory T cells (Tregs) are the key cells regulating peripheral autoreactive T lymphocytes. Tregs exert their function by suppressing efector T cells. Tregs have been shown to play essential roles in the control of a variety of physiological and pathological immune responses. However, Tregs are unstable and can lose the expression of FOXP3 and suppressive functions as a consequence of outer stimuli. Available literature suggests that secreted proteins regulate Treg functional states, such as diferentiation, proliferation and suppressive function. Identifcation of secreted proteins that afect Treg cell function are highly interesting for both therapeutic and diagnostic purposes in either hyperactive or immunosuppressed populations. Here, we report a phenotypic screening of a human secretome library in human Treg cells utilising a high throughput fow cytometry technology. Screening a library of 575 secreted proteins allowed us to identify proteins stabilising or destabilising the Treg phenotype as suggested by changes in expression of Treg marker proteins FOXP3 and/or CTLA4. Four proteins including GDF‑7, IL‑10, PAP and IFNα‑7 were identifed as positive regulators that increased FOXP3 and/or CTLA4 expression. PAP is a phosphatase. A catalytic‑dead version of the protein did not induce an increase in FOXP3 expression. -
Cells 1/IL-29) in Human Airway Epithelial Λ (IFN- 1 Promoter Activity
Regulation of IFN-λ1 Promoter Activity (IFN- λ1/IL-29) in Human Airway Epithelial Cells This information is current as Rachael Siegel, Joyce Eskdale and Grant Gallagher of September 27, 2021. J Immunol 2011; 187:5636-5644; Prepublished online 4 November 2011; doi: 10.4049/jimmunol.1003988 http://www.jimmunol.org/content/187/11/5636 Downloaded from References This article cites 48 articles, 19 of which you can access for free at: http://www.jimmunol.org/content/187/11/5636.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • 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 by guest on September 27, 2021 *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 © 2011 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Regulation of IFN-l1 Promoter Activity (IFN-l1/IL-29) in Human Airway Epithelial Cells Rachael Siegel, Joyce Eskdale, and Grant Gallagher The type III (l) IFNs (IFN-l1, IFN-l2, and IFN-l3) and their receptor are the most recently discovered IFN family. -
Affiliations
Supplementary material Proteome-wide survey of the autoimmune target repertoire in autoimmune polyendocrine syndrome type 1 *Nils Landegren1,2, Donald Sharon3,4, Eva Freyhult2,5,6,, Åsa Hallgren1,2, Daniel Eriksson1,2, Per-Henrik Edqvist7, Sophie Bensing8, Jeanette Wahlberg9, Lawrence M. Nelson10, Jan Gustafsson11, Eystein S Husebye12, Mark S Anderson13, Michael Snyder3, Olle Kämpe1,2 Nils Landegren and Donald Sharon contributed equally to the work Affiliations 1Department of Medicine (Solna), Karolinska University Hospital, Karolinska Institutet, Sweden 2Science for Life Laboratory, Department of Medical Sciences, Uppsala University, Sweden 3Department of Genetics, Stanford University, California, USA 4Department of Molecular, Cellular, and Developmental Biology, Yale University, Connecticut, USA 1 5Department of Medical Sciences, Cancer Pharmacology and Computational Medicine, Uppsala University 6Bioinformatics Infrastructure for Life Sciences 7Department of Immunology, Genetics and Pathology, Uppsala University, Sweden and Science for Life Laboratory 8 Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden 9Department of Endocrinology and Department of Medical and Health Sciences and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden 10Integrative Reproductive Medicine Group, Intramural Research Program on Reproductive and Adult Endocrinology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. 11Department -
Secreted Factors from Dental Pulp Stem Cells Improve Sjögren's Syndrome Via Regulatory T Cell-Mediated Immunosuppression
Matsumura-Kawashima et al. Stem Cell Research & Therapy (2021) 12:182 https://doi.org/10.1186/s13287-021-02236-6 RESEARCH Open Access Secreted factors from dental pulp stem cells improve Sjögren’s syndrome via regulatory T cell-mediated immunosuppression Mayu Matsumura-Kawashima†, Kenichi Ogata*† , Masafumi Moriyama, Yuka Murakami, Tatsuya Kawado and Seiji Nakamura Abstract Background: Sjögren’s syndrome (SS) is a chronic autoimmune disease primarily characterized by inflammation in the salivary and lacrimal glands. Activated T cells contribute to disease pathogenesis by producing proinflammatory cytokines, which leads to a positive feedback loop establishment. The study aimed to evaluate the effects of secreted factors derived from dental pulp stem cells (DPSCs) or bone marrow mesenchymal stem cells (BMMSCs) on hyposalivation in SS and to investigate the mechanism involved. Methods: Eighty percent confluent stem cells were replenished with serum-free Dulbecco’s modified Eagle’s medium and incubated for 48 h; following which, conditioned media from DPSCs (DPSC-CM) and BMMSCs (BMMSC-CM) were collected. Cytokine array analysis was performed to assess the types of cytokines present in the media. Flow cytometric analysis was performed to evaluate the number of activated T cells cultured in DPSC-CM or BMMSC-CM. Subsequently, DPSC-CM or BMMSC-CM was administered to an SS mouse model. The mice were categorized into the following groups (n = 6 each): non-treatment, Dulbecco’s modified Eagle’s medium (−), BMMSC-CM, and DPSC-CM. Histological analysis of the salivary glands was performed. The gene and protein expression levels of cytokines associated with T helper subsets in the submandibular glands (SMGs) were evaluated.