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: Analysis of C4 and the C4 binding protein in the MRL/lpr mouse. | Available online http content 9 5 R114 Open Access Research article Analysis of C4 and the C4 binding protein in the MRL lpr mouse Scott E Wenderfer1 2 Kipruto Soimo1 Rick A Wetsel1 and Michael C Braun1 2 Center for Immunology and Autoimmune Diseases Brown Foundation Institute of Molecular Medicine 1825 Pressler Street Houston TX 77030 USA 2Pediatric Nephrology University of Texas 6431 Fannin Street Houston TX 77030 USA Corresponding author Michael C Braun Received 15 Aug 2007 Revisions requested 12 Sep 2007 Revisions received 11 Oct 2007 Accepted 30 Oct 2007 Published 30 Oct 2007 Arthritis Research Therapy 2007 9 R114 doi ar2320 This article is online at http content 9 5 R114 2007 Wenderfer 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 Systemic lupus erythematosus is a complement-mediated autoimmune disease. While genetic deficiencies of classical pathway components lead to an increased risk of developing systemic lupus erythematosus end organ damage is associated with complement activation and immune complex deposition. The role of classical pathway regulators in systemic lupus erythematosus is unknown. C4 binding protein C4bp is a major negative regulator of the classical pathway. In order to study the role of C4bp deficiency in an established murine model of lupus nephritis mice with a targeted deletion in the gene encoding C4bp were backcrossed into the MRL lpr genetic background. Compared with control MRL lpr mice C4bp knockout MLR lpr mice had similar mortality and similar degrees of lymphoproliferation. There were no differences in the extent of proteinuria or renal inflammation. Staining for complement proteins and .
