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Journal List > J Biomed Biotechnol > v.2010; 2010 | Formats: * Abstract| * Full Text| * PDF (3.2M) |
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| J Biomed Biotechnol. 2010; 2010: 457146. Published online 2010 June 29. doi: 10.1155/2010/457146. | PMCID: PMC2910555 |
Copyright © 2010 Marco Tucci et al.CytokineOverproduction, T-Cell Activation, and Defective T-Regulatory Functions Promote Nephritis in Systemic Lupus ErythematosusMarco Tucci,* Stefania Stucci, Sabino Strippoli, and Francesco SilvestrisDIMO, Department of Internal Medicine and Clinical Oncology, University of Bari, Piazza Giulio Cesare 11, 70124 Bari, Italy*Marco Tucci: Email: m.tucci@dimo.uniba.itAcademic Editor: Brian PooleReceivedFebruary 5, 2010; Accepted March 15, 2010.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. *  Other Sections▼ * Abstract * 1. Introduction * 2. Pathogenetic Relevance of T-Cell Function in Lupus Nephritis * 3.Interleukin-17 Producing T-Cells * 4. Regulatory T-Cells and Dendritic Cells in Lupus Nephritis * 5. Conclusions * ReferencesAbstractLupus nephritis (LN) occurs in more than one-third of patients with systemic lupus erythematosus. Its pathogenesis is mostly attributable to the glomerular deposition of immune complexes and overproduction of T helper- (Th-) 1 cytokines. In this context, thehigh glomerular expression of IL-12 and IL-18 exerts a major pathogenetic role. These cytokines are locally produced by both macrophages and dendritic cells (DCs) which attract other inflammatory cells leading to maintenance of the kidney inflammation. However, other populations including T-cells and B-cells are integral for the development and worsening of renal damage. T-cells include manypathogenetic subsets, and the activation of Th-17 in keeping with defective T-regulatory (Treg) cell function regards as further event contributing to the glomerular damage. These populations also activate B-cells to produce nephritogenic auto-antibodies. Thus, LN includes a complex pathogenetic mechanism that involves different players and the evaluation of their activity may provide an effective toolfor monitoring the onset of the disease. *  Other Sections▼ * Abstract * 1. Introduction * 2. Pathogenetic Relevance of T-Cell Function in Lupus Nephritis * 3. Interleukin-17 Producing T-Cells * 4. Regulatory T-Cells and Dendritic Cells in Lupus Nephritis * 5. Conclusions * References1. IntroductionLupus nephritis (LN) is a major clinical manifestation ofsystemic lupus erythematosus that occurs in 15% of patients at diagnosis and in approximately 40% during the course of the disease. Renal biopsy is the gold standard for the diagnosis and follow-up, whereas the measurement of proteinuria identifies patients with overt renal failure, but fails to detect early silent disease. Thus, a better definition of the pathogenetic mechanisms leading to LN isrequired to identify effective markers of renal inflammation.LN is generally attributed to an intriguing interplay between renal parenchymal cells and inflammatory cells recruited in consequence of the deposition and/or in situ production of immune complexes (ICs) [1]. ICs increase the production of cytokines, chemokines, and adhesion molecules which allow the progressive infiltration of macrophages,dendritic cells (DCs) and T-cells resulting in chronic renal failure [2]. Moreover, cytokines and chemokines secreted by cells infiltrating glomeruli further promote the migration of other inflammatory cells that are attracted toward the inflammatory sites in response to a concentration gradient [3, 4].Notwithstanding SLE is considered a T helper- (Th-) 2 driven disease [5–7], experimental models...
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