IL1F10 Monoclonal Antibody

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Product Datasheet IL1F10 Monoclonal Antibody Catalog No: #42049 Orders: [email protected] Description Support: [email protected] Product Name IL1F10 Monoclonal Antibody Host Species Mouse Clonality Monoclonal Purification protein G purifed Applications IHC Species Reactivity Hu Specificity specific for Human IL1F10 denatured and native forms Immunogen Type protein Immunogen Description Recombinant Human IL1F10 protein Target Name IL1F10 Other Names IL-1F10, Family of interleukin 1-theta, FIL1 theta Interleukin-1 HY2, IL-1HY2, Interleukin-1 theta, IL-1 theta Interleukin-38, IL-38 Accession No. Swiss-Prot#: Q8WWZ1 Concentration 1.0mg/mL Formulation Preservative: 0.03% Proclin 300 Constituents: 50% Glycerol, 0.01M PBS, PH 7.4 Storage Store at -20°C Application Details Immunohistochemistry: 1:20 - 1:200 Images Immunohistochemical analysis of paraffin-embedded Human Colon cancer tissue using #42049 at dilution of 1:200. Address: 8400 Baltimore Ave. Suite 302 College Park MD 20740 USA http://www.sabbiotech.com 1 Immunohistochemical analysis of paraffin-embedded Human live cancer tissue using #42049 at dilution of 1:200. Immunohistochemical analysis of paraffin-embedded Human spleen tissue using #42049 at dilution of 1:200. Background Cytokine with immunomodulatory activity. Alone, does not induce cytokine production, but reduces IL22 and IL17A production by T-cells in response to heat-killed Candida albicans. Reduces IL36G-induced production of IL8 by peripheral blood mononuclear cells. Increases IL6 production by dendritic cells stimulated by bacterial lipopolysaccharides (LPS). Ligand for IL-36R/IL1RL2. References "IL-38 binds to the IL-36 receptor and has biological effects on immune cells similar to IL-36 receptor antagonist." van de Veerdonk F.L., Stoeckman A.K., Wu G., Boeckermann A.N., Azam T., Netea M.G., Joosten L.A., van der Meer J.W., Hao R., Kalabokis V., Dinarello C.A. Proc. Natl. Acad. Sci. U.S.A. 109:3001-3005(2012) [PubMed] [Europe PMC] [Abstract] Cited for: FUNCTION. Note: This product is for in vitro research use only and is not intended for use in humans or animals. Address: 8400 Baltimore Ave. Suite 302 College Park MD 20740 USA http://www.sabbiotech.com 2.

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Wo 2010/075007 A2
(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 1 July 2010 (01.07.2010) WO 2010/075007 A2 (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every C12Q 1/68 (2006.01) G06F 19/00 (2006.01) kind of national protection available): AE, AG, AL, AM, C12N 15/12 (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) International Application Number: DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, PCT/US2009/067757 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, 11 December 2009 ( 11.12.2009) 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, TJ, TM, TN, TR, TT, (26) Publication Language: English TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (30) Priority Data: (84) Designated States (unless otherwise indicated, for every 12/3 16,877 16 December 2008 (16.12.2008) US kind of regional protection available): ARIPO (BW, GH, GM, KE, LS, MW, MZ, NA, SD, SL, SZ, TZ, UG, ZM, (71) Applicant (for all designated States except US): DODDS, ZW), Eurasian (AM, AZ, BY, KG, KZ, MD, RU, TJ, W., Jean [US/US]; 938 Stanford Street, Santa Monica, TM), European (AT, BE, BG, CH, CY, CZ, DE, DK, EE, CA 90403 (US).
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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
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Huil36g 169 Data Sheet
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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
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Published OnlineFirst February 18, 2016; DOI: 10.1158/0008-5472.CAN-15-1548 Cancer Tumor and Stem Cell Biology Research Inflammation-Dependent IL18 Signaling Restricts Hepatocellular Carcinoma Growth by Enhancing the Accumulation and Activity of Tumor- Infiltrating Lymphocytes Geoffrey J. Markowitz1, Pengyuan Yang1,2,3, Jing Fu3, Gregory A. Michelotti4, Rui Chen1, Jianhua Sui5, Bin Yang2, Wen-Hao Qin3, Zheng Zhang6, Fu-Sheng Wang6, Anna Mae Diehl4, Qi-Jing Li7, Hongyang Wang3, and Xiao-Fan Wang1 Abstract Chronic inflammation in liver tissue is an underlying cause of IL18R1 deletion increased tumor burden. Mechanistically, we hepatocellular carcinoma. High levels of inflammatory cytokine foundthatIL18exertedinflammation-dependent tumor-sup- IL18 in the circulation of patients with hepatocellular carcinoma pressive effects largely by promoting the differentiation, activ- correlates with poor prognosis. However, conflicting results have ity, and survival of tumor-infiltrating T cells. Finally, differences been reported for IL18 in hepatocellular carcinoma development in the expression of IL18 in tumor tissue versus nontumor and progression. In this study, we used tissue specimens from tissueweremorepredictiveofpatientoutcomethanoverall hepatocellular carcinoma patients and clinically relevant mouse tissue expression. Taken together, our findings resolve a long- models of hepatocellular carcinoma to evaluate IL18 expression standing contradiction regarding a tumor-suppressive role for and function. In a mouse model of liver fibrosis that recapitulates IL18 in established hepatocellular carcinoma and provide a a tumor-promoting microenvironment, global deletion of the mechanistic explanation for the complex relationship between IL18 receptor IL18R1 enhanced tumor growth and burden. Sim- its expression pattern and hepatocellular carcinoma prognosis. ilarly, in a carcinogen-induced model of liver tumorigenesis, Cancer Res; 76(8); 1–12.
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Comprehensive Association Study of Genetic Variants in the IL-1 Gene Family in Systemic Juvenile Idiopathic Arthritis
Genes and Immunity (2008) 9, 349–357 & 2008 Nature Publishing Group All rights reserved 1466-4879/08 $30.00 www.nature.com/gene ORIGINAL ARTICLE Comprehensive association study of genetic variants in the IL-1 gene family in systemic juvenile idiopathic arthritis CJW Stock1, EM Ogilvie1, JM Samuel1, M Fife1, CM Lewis2 and P Woo1 1Centre for Paediatric and Adolescent Rheumatology, Windeyer Institute for Medical Sciences, University College London, London, UK and 2Guy’s, Kings and St Thomas’ School of Medicine, London, UK Patients with systemic juvenile idiopathic arthritis (sJIA) have a characteristic daily spiking fever and elevated levels of inflammatory cytokines. Members of the interleukin-1 (IL-1) gene family have been implicated in various inflammatory and autoimmune diseases, and treatment with the IL-1 receptor antagonist, Anakinra, shows remarkable improvement in some patients. This work describes the most comprehensive investigation to date of the involvement of the IL-1 gene family in sJIA. A two-stage case–control association study was performed to investigate the two clusters of IL-1 family genes using a tagging single nucleotide polymorphism (SNP) approach. Genotyping data of 130 sJIA patients and 151 controls from stage 1 highlighted eight SNPs in the IL1 ligand cluster region and two SNPs in the IL1 receptor cluster region as showing a significant frequency difference between the populations. These 10 SNPs were typed in an additional 105 sJIA patients and 184 controls in stage 2. Meta-analysis of the genotypes from both stages showed that three IL1 ligand cluster SNPs (rs6712572, rs2071374 and rs1688075) and one IL1 receptor cluster SNP (rs12712122) show evidence of significant association with sJIA.
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WO 2018/067991 Al 12 April 2018 (12.04.2018) W !P O PCT
(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 WO 2018/067991 Al 12 April 2018 (12.04.2018) W !P O PCT (51) International Patent Classification: achusetts 021 15 (US). THE BROAD INSTITUTE, A61K 51/10 (2006.01) G01N 33/574 (2006.01) INC. [US/US]; 415 Main Street, Cambridge, Massachu C07K 14/705 (2006.01) A61K 47/68 (2017.01) setts 02142 (US). MASSACHUSETTS INSTITUTE OF G01N 33/53 (2006.01) TECHNOLOGY [US/US]; 77 Massachusetts Avenue, Cambridge, Massachusetts 02139 (US). (21) International Application Number: PCT/US2017/055625 (72) Inventors; and (71) Applicants: KUCHROO, Vijay K. [IN/US]; 30 Fairhaven (22) International Filing Date: Road, Newton, Massachusetts 02149 (US). ANDERSON, 06 October 2017 (06.10.2017) Ana Carrizosa [US/US]; 110 Cypress Street, Brookline, (25) Filing Language: English Massachusetts 02445 (US). MADI, Asaf [US/US]; c/o The Brigham and Women's Hospital, Inc., 75 Francis (26) Publication Language: English Street, Boston, Massachusetts 021 15 (US). CHIHARA, (30) Priority Data: Norio [US/US]; c/o The Brigham and Women's Hospital, 62/405,835 07 October 2016 (07.10.2016) US Inc., 75 Francis Street, Boston, Massachusetts 021 15 (US). REGEV, Aviv [US/US]; 15a Ellsworth Ave, Cambridge, (71) Applicants: THE BRIGHAM AND WOMEN'S HOSPI¬ Massachusetts 02139 (US). SINGER, Meromit [US/US]; TAL, INC. [US/US]; 75 Francis Street, Boston, Mass c/o The Broad Institute, Inc., 415 Main Street, Cambridge, (54) Title: MODULATION OF NOVEL IMMUNE CHECKPOINT TARGETS CD4 FIG.
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IL-17-Producing Cells in Tumor Immunity: Friends Or Foes?
Immune Netw. 2020 Feb;20(1):e6 https://doi.org/10.4110/in.2020.20.e6 pISSN 1598-2629·eISSN 2092-6685 Review Article IL-17-Producing Cells in Tumor Immunity: Friends or Foes? Da-Sol Kuen 1,2, Byung-Seok Kim 1, Yeonseok Chung 1,2,* 1Laboratory of Immune Regulation, Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Korea 2BK21 Plus Program, Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Korea Received: Dec 29, 2019 Revised: Jan 25, 2020 ABSTRACT Accepted: Jan 26, 2020 IL-17 is produced by RAR-related orphan receptor gamma t (RORγt)-expressing cells *Correspondence to including Th17 cells, subsets of γδT cells and innate lymphoid cells (ILCs). The biological Yeonseok Chung significance of IL-17-producing cells is well-studied in contexts of inflammation, Laboratory of Immune Regulation and BK21 Plus Program, Institute of Pharmaceutical autoimmunity and host defense against infection. While most of available studies in tumor + Sciences, Seoul National University, 1 Gwanak- immunity mainly focused on the role of T-bet-expressing cells, including cytotoxic CD8 ro, Gwanak-gu, Seoul 08826, Korea. T cells and NK cells, and their exhaustion status, the role of IL-17-producing cells remains E-mail: [email protected] poorly understood. While IL-17-producing T-cells were shown to be anti-tumorigenic in Copyright © 2020. The Korean Association of adoptive T-cell therapy settings, mice deficient in type 17 genes suggest a protumorigenic Immunologists potential of IL-17-producing cells. This review discusses the features of IL-17-producing This is an Open Access article distributed cells, of both lymphocytic and myeloid origins, as well as their suggested pro- and/or anti- under the terms of the Creative Commons tumorigenic functions in an organ-dependent context.
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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.
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Decrease in Mucosal IL17A, IFN and IL10 Expressions in Active Crohn's
nutrients Article Decrease in Mucosal IL17A, IFNγ and IL10 Expressions in Active Crohn’s Disease Patients Treated with High-Dose Vitamin D Alone or Combined with Infliximab Mia Bendix 1,*, Anders Dige 1, Søren Peter Jørgensen 1, Jens Frederik Dahlerup 1 , Bo Martin Bibby 2, Bent Deleuran 3,4 and Jørgen Agnholt 1 1 Department of Hepatology and Gastroenterology, Aarhus University Hospital, 8200 Aarhus, Denmark; [email protected] (A.D.); [email protected] (S.P.J.); [email protected] (J.F.D.); [email protected] (J.A.) 2 Department of Public Health—Department of Biostatistics, Aarhus University, 8000 Aarhus, Denmark; [email protected] 3 Department of Rheumatology, Aarhus University Hospital, 8200 Aarhus, Denmark; [email protected] 4 Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark * Correspondence: [email protected] Received: 5 November 2020; Accepted: 26 November 2020; Published: 30 November 2020 Abstract: Background: Vitamin D treatment may reduce Crohn’s disease (CD) activity by modulating the mucosal immune function. We investigated if high-dose vitamin D +/ infliximab modulated − the mucosal cytokine expression in active CD. Methods: Forty CD patients were randomized into: infliximab + vitamin D; infliximab + placebo-vitamin D; placebo-infliximab + vitamin D or placebo-infliximab + placebo-vitamin D. Infliximab (5 mg/kg) and placebo-infliximab were administered at weeks 0, 2 and 6. Oral vitamin D was administered as bolus 200,000 international units (IU) per week 0 followed by 20,000 IU/day for 7 weeks or placebo. Endoscopy with biopsies was performed at weeks 0 and 7 where endoscopic activity was measured and mucosal mRNA cytokine expression was examined.
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