Interleukin-15 Expression Affects Homeostasis and Function of B Cells Through NK Cell-Derived Interferon-C
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Type I Interferons and the Development of Impaired Vascular Function and Repair in Human and Murine Lupus
Type I Interferons and the Development of Impaired Vascular Function and Repair in Human and Murine Lupus by Seth G Thacker A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Immunology) in The University of Michigan 2011 Doctoral Committee: Associate Professor Mariana J. Kaplan, Chair Professor David A. Fox Professor Alisa E. Koch Professor Matthias Kretzler Professor Nicholas W. Lukacs Associate Professor Daniel T. Eitzman © Seth G Thacker 2011 Sharon, this work is dedicated to you. This achievement is as much yours as it is mine. Your support through all six years of this Ph.D. process has been incredible. You put up with my countless miscalculations on when I would finish experiments, and still managed to make me and our kids feel loved and special. Without you this would have no meaning. Sharon, you are the safe harbor in my life. ii Acknowledgments I have been exceptionally fortunate in my time here at the University of Michigan. I have been able to interact with so many supportive people over the years. I would like to express my thanks and admiration for my mentor. Mariana has taught me so much about writing, experimental design and being a successful scientist in general. I could never have made it here without her help. I would also like to thank Mike Denny. He had a hand in the beginning of all of my projects in one way or another, and was always quick and eager to help in whatever way he could. He really made my first year in the lab successful. -
Huil36g 169 Data Sheet
Growth Factor Data Sheet GoldBio growth factors are manufactured for RESEARCH USE ONLY and cannot be sold for human consumption! Interleukin-36G (IL36G) is a pro-inflammatory cytokine that plays an important role in the pathophysiology of several diseases. IL36A, IL36B and IL36G; (formerly IL1F6, IL1F8, and IL1F9) are IL1 family members that signal through the IL1 receptor family members IL1Rrp2 (IL1RL2) and IL1RAcP. IL36B is secreted when transfected into 293-T cells and could constitute part of an independent signaling system analogous to that of IL1A and IL1B receptor agonist and interleukin-1 receptor type I (IL1R1). Furthermore, IL36G also can function as an agonist of NFκB activation through the orphan IL1- receptor-related protein 2. Recombinant human IL36G is synthesized as a protein that contains no signal sequence, no prosegment and no potential N-linked glycosylation site.There is a 53% amino acid homology between human and mouse IL36G. IL36G also has a 25-55% amino acid homology with IL36G and IL1RN, IL1B, IL36RN, IL36A, IL37, IL36B and IL1F10. Catalog Number 1110-36E Product Name IL36G (IL-36 gamma), Human (169 a.a.) Recombinant Human Interleukin-36γ IL36G, IL36γ Interleukin 1 Homolog 1 (IL1H1) Interleukin 1-Related Protein 2 (IL1RP2) Interleukin 1 Family, Member 9 (IL1F9) Source Escherichia coli MW 18.7 kDa (169 amino acids) Sequence MRGTPGDADG GGRAVYQSMC KPITGTINDL NQQVWTLQGQ NLVAVPRSDS VTPVTVAVIT CKYPEALEQG RGDPIYLGIQ NPEMCLYCEK VGEQPTLQLK EQKIMDLYGQ PEPVKPFLFY RAKTGRTSTL ESVAFPDWFI ASSKRDQPII LTSELGKSYN TAFELNIND Accession Number Q9NZH8 Purity >95% by SDS-PAGE and HPLC analyses Biological Activity Fully biologically active when compared to standard. The specific activity is determined by its binding ability in a functional ELISA. -
Interleukin (IL)17A, F and AF in Inflammation: a Study in Collageninduced Arthritis and Rheumatoid Arthritis
bs_bs_banner Clinical and Experimental Immunology ORIGINAL ARTICLE doi:10.1111/cei.12376 Interleukin (IL)-17A, F and AF in inflammation: a study in collagen-induced arthritis and rheumatoid arthritis S. Sarkar,* S. Justa,* M. Brucks,* Summary J. Endres,† D. A. Fox,† X. Zhou,* Interleukin (IL)-17 plays a critical role in inflammation. Most studies to date F. Alnaimat,* B. Whitaker,‡ have elucidated the inflammatory role of IL-17A, often referred to as IL-17. J. C. Wheeler,‡ B. H. Jones§ and IL-17F is a member of the IL-17 family bearing 50% homology to IL-17A S. R. Bommireddy* and can also be present as heterodimer IL-17AF. This study elucidates the *Section of Rheumatology, Department of Medicine, and the Arizona Arthritis Center, distribution and contribution of IL-17A, F and AF in inflammatory arthritis. University of Arizona, Tucson, AZ, †Divison of Neutralizing antibody to IL-17A alone or IL-17F alone or in combination Rheumatology, Department of Internal Medicine, was utilized in the mouse collagen-induced arthritis (CIA) model to eluci- University of Michigan, Ann Arbor, MI, and date the contribution of each subtype in mediating inflammation. IL-17A, F ‡Biologics Research and §Immunology Discovery and AF were all increased during inflammatory arthritis. Neutralization of Research, Janssen Research and Development, IL-17A reduced the severity of arthritis, neutralization of IL-17A+IL-17F had Spring House, PA, USA the same effect as neutralizing IL-17A, while neutralization of IL-17F had no effect. Moreover, significantly higher levels of IL-17A and IL-17F were detected in peripheral blood mononuclear cells (PBMC) from patients with rheumatoid arthritis (RA) in comparison to patients with osteoarthritis (OA). -
Interleukin 2 Medical Intensive Care Unit (4MICU)
Interleukin 2 Medical Intensive Care Unit (4MICU) Ronald Reagan UCLA Medical Center 757 Westwood Plaza Los Angeles, CA 90095 Main Phone: (310) 267-7441 Fax: (310) 267-3785 About Our Unit The Medical Intensive Care Unit (MICU) cares Quick for critically ill patients in an intensive care Reference Guide environment, with nursing staff specially trained in the administration of Interleukin 2 therapy. Unit Director / Manager Mark Flitcraft, RN, MSN One registered nurse (RN) is assigned to take (310) 267-9529 care of a maximum of two patients. Our Medical Clinical Nurse Specialist Intensive Care Unit patient rooms are designed Yuhan Kao, RN, MSN, CNS (310) 267-7465 to allow nurses constant visual contact with their patients. As a safety precaution, the Medical Assistant Manager Sherry Xu, RN, BA, CCRN Intensive Care Unit is a closed unit and requires (310) 267-7485 permission to enter by intercom. Clinical Case Manager Each private-patient-care room contains the Connie Lefevre (310) 267-9740 most advanced intensive-care equipment available, including cardiac-monitoring and Clinical Social Worker Codie Lieto emergency-response equipment. The curtains in (310) 267-9741 the room will usually be drawn to keep your room Charge Nurse On-Duty more private. (310) 267-7480 or (310) 267-7482 A brief tour is available on weekdays for patients and visitors interested in walking through the unit Patient Affairs (310) 267-9113 and meeting the staff before arrival. To arrange for a tour, please call the nurse manager at Respiratory Supervisor (310) 267-9529. Orna Molayeme, MA, RCP, RRT, NPS (310) 267-8921 UCLAHEALTH.ORG 1-800-UCLA-MD1 (1-800-825-2631) About Our Unit During Your Stay Quick The Medical Team Reference Guide During each shift, you will be assigned a registered nurse (RN) and a clinical care partner (CCP). -
IL36G Blocking Peptide (CDBP5559) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use
IL36G blocking peptide (CDBP5559) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Antigen Description The protein encoded by this gene is a member of the interleukin 1 cytokine family. The activity of this cytokine is mediated by interleukin 1 receptor-like 2 (IL1RL2/IL1R-rp2), and is specifically inhibited by interleukin 1 family, member 5 (IL1F5/IL-1 delta). Interferon-gamma, tumor necrosis factor-alpha and interleukin 1, beta (IL1B) are reported to stimulate the expression of this cytokine in keratinocytes. The expression of this cytokine in keratinocytes can also be induced by a contact hypersensitivity reaction or herpes simplex virus infection. This gene and eight other interleukin 1 family genes form a cytokine gene cluster on chromosome 2. Two alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jun 2013] Immunogen 13 amino acids near the carboxy terminus of human IL-36G. Nature Synthetic Expression System N/A Species Reactivity Human Conjugate Unconjugated Applications Used as a blocking peptide in immunoblotting applications. Procedure None Format Liquid Concentration 200 μg/mL Size 0.05mg Preservative None Storage -20°C ANTIGEN GENE INFORMATION Gene Name IL36G interleukin 36, gamma [ Homo sapiens (human) ] Official Symbol IL36G 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved Synonyms IL36G; interleukin -
Growth Factor Data Sheet
Growth Factor Data Sheet GoldBio growth factors are manufactured for RESEARCH USE ONLY and cannot be sold for human consumption! Interleukin 36B (IL36B) is a pro-inflammatory cytokine which plays an important role in the pathophysiology of several diseases. IL36A, IL36B, and IL36G (formerly IL1F6, IL1F8, and IL1F9) are all IL1 family members that signal through the IL1 receptor family members IL1Rrp2 (IL1RL2) and IL1RAcP. IL36B is reported to be expressed at higher levels in psoriatic plaques than in symptomless psoriatic skin or healthy control skin. IL36B can also stimulate the production of IL6 and IL8 in synovial fibroblasts, articular chondrocytes and mature adipocytes. Catalog Number 1310-36D Product Name IL36B (IL-36 beta), Murine (153 a.a.) Recombinant Murine Interleukin-36β IL36B, IL36β Interleukin 36β Interleukin 1 Family, Member 8 (IL1F8) Source Escherichia coli MW ~17.4 kDa (153 amino acids) Sequence RAASPSLRHV QDLSSRVWIL QNNILTAVPR KEQTVPVTIT LLPCQYLDTL ETNRGDPTYM GVQRPMSCLF CTKDGEQPVL QLGEGNIMEM YNKKEPVKAS LFYHKKSGTT STFESAAFPG WFIAVCSKGS CPLILTQELG EIFITDFEMI VVH Purity >95% by SDS-PAGE and HPLC analyses Biological Activity Fully biologically active when compared to standard. The ED50 as determined by inducing IL-6 secretion in murine NIH/3T3 cells is less than 25 ng/ml, corresponding to a specific activity of >4.0 × 104 IU/mg. Formulation Sterile filtered white lyophilized powder. Purified and tested for use in cell culture. Storage/Handling This lyophilized preparation is stable at 2-8°C, but should be kept at -20°C for long term storage. The reconstituted sample can be apportioned into working aliquots and stored at -80 °C for up to 6 months. -
The Combination of IL-12 and IL-18 NK/T-NK Cells Derived with IL-2, IL-15
Cytokine Production and Killer Activity of NK/T-NK Cells Derived with IL-2, IL-15, or the Combination of IL-12 and IL-18 This information is current as Bernard R. Lauwerys, Nathalie Garot, Jean-Christophe of September 28, 2021. Renauld and Frédéric A. Houssiau J Immunol 2000; 165:1847-1853; ; doi: 10.4049/jimmunol.165.4.1847 http://www.jimmunol.org/content/165/4/1847 Downloaded from References This article cites 31 articles, 17 of which you can access for free at: http://www.jimmunol.org/content/165/4/1847.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 28, 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 © 2000 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Cytokine Production and Killer Activity of NK/T-NK Cells Derived with IL-2, IL-15, or the Combination of IL-12 and IL-181 Bernard R. Lauwerys,* Nathalie Garot,* Jean-Christophe Renauld,†‡ and Fre´de´ric A. -
The Role of Interleukin-1 Cytokine Family (IL-1Β, IL-37) and Interleukin-12 Cytokine
bioRxiv preprint doi: https://doi.org/10.1101/502609; this version posted December 22, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 Title: 2 The Role of Interleukin-1 cytokine family (IL-1β, IL-37) and interleukin-12 cytokine 3 family (IL-12, IL-35) in eumycetoma infection pathogenesis. 4 5 6 Authors 7 Amir Abushouk1,2, Amre Nasr1,2,3, Emad Masuadi4, Gamal Allam5,6, Emmanuel E. Siddig7, 8 Ahmed H. Fahal7 9 10 1Department of Basic Medical Sciences, College of Medicine, King Saud Bin Abdul-Aziz 11 University for Health Sciences, Jeddah, Kingdom of Saudi Arabia. E. mail: shouka@ksau- 12 hs.edu.sa 13 14 2King Abdullah International Medical Research Centre, National Guard Health Affairs, 15 Kingdom of Saudi Arabia. 16 17 3Department of Microbiology, College of Sciences and Technology, Al-Neelain University, 18 P.O. Box 1027, Khartoum, Sudan. [email protected] 19 20 4Research Unit, Department of Medical Education, College of Medicine-Riyadh, King Saud 21 Bin Abdul-Aziz University for Health Sciences, Riyadh, Kingdom of Saudi Arabia. E. mail: 22 [email protected] 23 bioRxiv preprint doi: https://doi.org/10.1101/502609; this version posted December 22, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. -
Interleukin-18 in Health and Disease
International Journal of Molecular Sciences Review Interleukin-18 in Health and Disease Koubun Yasuda 1 , Kenji Nakanishi 1,* and Hiroko Tsutsui 2 1 Department of Immunology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan; [email protected] 2 Department of Surgery, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan; [email protected] * Correspondence: [email protected]; Tel.: +81-798-45-6573 Received: 21 December 2018; Accepted: 29 January 2019; Published: 2 February 2019 Abstract: Interleukin (IL)-18 was originally discovered as a factor that enhanced IFN-γ production from anti-CD3-stimulated Th1 cells, especially in the presence of IL-12. Upon stimulation with Ag plus IL-12, naïve T cells develop into IL-18 receptor (IL-18R) expressing Th1 cells, which increase IFN-γ production in response to IL-18 stimulation. Therefore, IL-12 is a commitment factor that induces the development of Th1 cells. In contrast, IL-18 is a proinflammatory cytokine that facilitates type 1 responses. However, IL-18 without IL-12 but with IL-2, stimulates NK cells, CD4+ NKT cells, and established Th1 cells, to produce IL-3, IL-9, and IL-13. Furthermore, together with IL-3, IL-18 stimulates mast cells and basophils to produce IL-4, IL-13, and chemical mediators such as histamine. Therefore, IL-18 is a cytokine that stimulates various cell types and has pleiotropic functions. IL-18 is a member of the IL-1 family of cytokines. IL-18 demonstrates a unique function by binding to a specific receptor expressed on various types of cells. -
BAFF Suppresses IL-15 Expression in B Cells
BAFF Suppresses IL-15 Expression in B Cells Ning Ma, Chen Xing, He Xiao, Youdi He, Gencheng Han, Guojiang Chen, Chunmei Hou, Bernadette Marrero, Yujuan Wang, Shengquan Zhang, Beifen Shen, Yan Li and Renxi This information is current as Wang of September 28, 2021. J Immunol 2014; 192:4192-4201; Prepublished online 26 March 2014; doi: 10.4049/jimmunol.1302132 http://www.jimmunol.org/content/192/9/4192 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2014/03/26/jimmunol.130213 Material 2.DCSupplemental http://www.jimmunol.org/ References This article cites 39 articles, 14 of which you can access for free at: http://www.jimmunol.org/content/192/9/4192.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 28, 2021 • 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 All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology BAFF Suppresses IL-15 Expression in B Cells Ning Ma,*,†,1 Chen Xing,*,1 He Xiao,*,1 Youdi He,‡ Gencheng Han,* Guojiang Chen,* Chunmei Hou,* Bernadette Marrero,x Yujuan Wang,{ Shengquan Zhang,‖ Beifen Shen,* Yan Li,* and Renxi Wang* Clinical trials have shown that BAFF inhibitors do not reduce memory B cell levels but can reduce the number of mature B cells. -
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. -
Reduced Concentrations of the B Cell Cytokine Interleukin 38 Are Associated with Cardiovascular Disease Risk in Overweight Subjects
Eur. J. Immunol. 2020. 00: 1–10 DOI: 10.1002/eji.201948390 Dennis M. de Graaf et al. 1 Clinical Allergy and inflammation Research Article Reduced concentrations of the B cell cytokine interleukin 38 are associated with cardiovascular disease risk in overweight subjects DennisM.deGraaf1,2 , Martin Jaeger2 ,IngeC.L.vanden Munckhof2 , Rob ter Horst2 ,KikiSchraa2 , Jelle Zwaag3 , Matthijs Kox3 , Mayumi Fujita4 , Takeshi Yamauchi4, Laura Mercurio5 , Stefania Madonna5 , Joost H.W. Rutten2 , Jacqueline de Graaf2 ,NielsP.Riksen2 , Frank L. van de Veerdonk2 , Mihai G. Netea2 , Leo A.B. Joosten2 and Charles A. Dinarello1,2 1 Department of Medicine, University of Colorado Denver, Aurora, CO, USA 2 Department of Internal Medicine and Radboud Institute of Molecular Life Science (RIMLS), Radboud University Medical Center, Nijmegen, The Netherlands 3 Department of Intensive Care Medicine and Radboud Institute of Molecular Life Science (RIMLS), Radboud University Medical Center, Nijmegen, The Netherlands 4 Department of Dermatology, University of Colorado Denver, Aurora, CO, USA 5 Laboratory of Experimental Immunology, IDI-IRCCSFondazione Luigi M. Monti, Rome, Italy The IL-1 family member IL-38 (IL1F10) suppresses inflammatory and autoimmune con- ditions. Here, we report that plasma concentrations of IL-38 in 288 healthy Europeans correlate positively with circulating memory B cells and plasmablasts. IL-38 correlated negatively with age (p = 0.02) and was stable in 48 subjects for 1 year. In comparison with primary keratinocytes, IL1F10 expression in CD19+ B cells from PBMC was lower, whereas cell-associated IL-38 expression was comparable. In vitro, IL-38 is released from CD19+ B cells after stimulation with rituximab.