Báo cáo y học: "Type I interferon receptor controls B-cell expression of nucleic acid-sensing Toll-like receptors and autoantibody production in a murine model of lupus"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Type I interferon receptor controls B-cell expression of nucleic acid-sensing Toll-like receptors and autoantibody production in a murine model of lupus. | Available online http content 11 4 R112 Open Access Research article Type I interferon receptor controls B-cell expression of nucleic acid-sensing Toll-like receptors and autoantibody production in a murine model of lupus Donna L Thibault1 2 Kareem L Graham1 Lowen Y Lee1 Imelda Balboni1 3 Paul J Hertzog4 and Paul J Utz1 Department of Medicine Division of Immunology and Rheumatology Stanford University School of Medicine 269 Campus Drive CCSR 2250 Stanford CA 94305 USA 2Current address Genentech Inc. 1 DNA Way South San Francisco CA 94080 USA department of Pediatrics Division of Pediatric Rheumatology Stanford University School of Medicine 300 Pasteur Drive Boswell Building A085 Stanford CA 94305 USA 4Centre for Functional Genomics and Human Disease Monash Institute of Medical Research 27-31 Wright Street Clayton Victoria 3168 Australia Corresponding author Donna L Thibault Received 25 Feb 2009 Revisions requested 3 Apr 2009 Revisions received 22 May 2009 Accepted 22 Jul 2009 Published 22 Jul 2009 Arthritis Research Therapy 2009 11 R112 doi 86 ar2771 This article is online at http content 11 4 R112 2009 Thibault et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Introduction Systemic lupus erythematosus SLE is a chronic autoimmune disease characterized by the production of high-titer IgG autoantibodies directed against nuclear autoantigens. Type I interferon IFN-I has been shown to play a pathogenic role in this disease. In the current study we characterized the role of the IFNAR2 chain of the type I IFN IFN-I receptor in the targeting of nucleic acid-associated autoantigens and in B-cell expression of the nucleic acid-sensing Toll-like

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