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Autoimmune Dis. 2012; 2012: 849684.
Published online Mar 22, 2012. doi:  10.1155/2012/849684
PMCID: PMC3318208
Lupus Nephritis: An Overview of Recent Findings
Alberto de Zubiria Salgado 1 ,2 and Catalina Herrera-Diaz 2 *
1Department of Internal Medicine and Clinical Immunology, The Samaritan University Hospital, Bogotá, Colombia
2Center for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Carrera 24 No. 63C-69, Bogotá, Colombia
*Catalina Herrera-Diaz: catalina.herrera.doc.medicina/at/gmail.com
Academic Editor: Mario García-Carrasco
Received October 15, 2011; Accepted November 30, 2011.
Abstract
Lupus nephritis (LN) is one of the most serious complications of systemic lupus erythematosus (SLE) since it is the major predictor of poor prognosis. In susceptible individuals suffering of SLE, in situ formation and deposit of immune complexes (ICs) from apoptotic bodies occur in the kidneys as a result of an amplified epitope immunological response. IC glomerular deposits generate release of proinflammatory cytokines and cell adhesion molecules causing inflammation. This leads to monocytes and polymorphonuclear cells chemotaxis. Subsequent release of proteases generates endothelial injury and mesangial proliferation. Presence of ICs promotes adaptive immune response and causes dendritic cells to release type I interferon. This induces maturation and activation of infiltrating T cells, and amplification of Th2, Th1 and Th17 lymphocytes. Each of them, amplify B cells and activates macrophages to release more proinflammatory molecules, generating effector cells that cannot be modulated promoting kidney epithelial proliferation and fibrosis. Herein immunopathological findings of LN are reviewed.
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