狼疮行性肾炎教案.pdfVIP

Hindawi Publishing Corporation Clinical and Developmental Immunology Volume 2012, Article ID 139365, 13 pages doi:10.1155/2012/139365 Review Article Autoantibodies and Resident Renal Cells in the Pathogenesis of Lupus Nephritis : Getting to Know the Unknown Susan Yung and Tak Mao Chan Department of Medicine, Queen Mary Hospital, University of Hong Kong, Pokfulam, Hong Kong Correspondence should be addressed to Susan Yung, ssyyung@hku.hk and Tak Mao Chan, dtmchan@hku.hk Received 20 February 2012; Accepted 26 March 2012 Academic Editor: Chaim Putterman Copyright © 2012 S. Yung and T. M. Chan. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Systemic lupus erythematosus is characterized by a breakdown of self-tolerance and production of autoantibodies. Kidney involvement (i.e., lupus nephritis) is both common and severe and can result in permanent damage within the glomerular, vascular, and tubulo-interstitial compartments of the kidney, leading to acute or chronic renal failure. Accumulating evidence shows that anti-dsDNA antibodies play a critical role in the pathogenesis of lupus nephritis through their binding to cell surface proteins of resident kidney cells, thereby triggering the downstream activation of signaling pathways and the release of mediators of inflammation and fibrosis. This paper describes the mechanisms through which autoantibodies interact with resident renal cells and how this interaction plays a part in disease pathogenesis that ultimately leads to structural and functional alterations in lupus nephritis. 1. Introduction