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Cytokine Overproduction, T-Cell Activation, and Defective T-Regulatory Functions Promote Nephritis in Systemic Lupus Erythematosus
Lupus 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, the high glomerular expression of IL-12 and I...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910555/ https://www.ncbi.nlm.nih.gov/pubmed/20671931 http://dx.doi.org/10.1155/2010/457146 |
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author | Tucci, Marco Stucci, Stefania Strippoli, Sabino Silvestris, Francesco |
author_facet | Tucci, Marco Stucci, Stefania Strippoli, Sabino Silvestris, Francesco |
author_sort | Tucci, Marco |
collection | PubMed |
description | Lupus 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, the high 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 many pathogenetic 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 tool for monitoring the onset of the disease. |
format | Text |
id | pubmed-2910555 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-29105552010-07-29 Cytokine Overproduction, T-Cell Activation, and Defective T-Regulatory Functions Promote Nephritis in Systemic Lupus Erythematosus Tucci, Marco Stucci, Stefania Strippoli, Sabino Silvestris, Francesco J Biomed Biotechnol Review Article Lupus 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, the high 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 many pathogenetic 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 tool for monitoring the onset of the disease. Hindawi Publishing Corporation 2010 2010-06-29 /pmc/articles/PMC2910555/ /pubmed/20671931 http://dx.doi.org/10.1155/2010/457146 Text en Copyright © 2010 Marco Tucci et al. 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. |
spellingShingle | Review Article Tucci, Marco Stucci, Stefania Strippoli, Sabino Silvestris, Francesco Cytokine Overproduction, T-Cell Activation, and Defective T-Regulatory Functions Promote Nephritis in Systemic Lupus Erythematosus |
title | Cytokine Overproduction, T-Cell Activation, and Defective T-Regulatory Functions Promote Nephritis in Systemic Lupus Erythematosus |
title_full | Cytokine Overproduction, T-Cell Activation, and Defective T-Regulatory Functions Promote Nephritis in Systemic Lupus Erythematosus |
title_fullStr | Cytokine Overproduction, T-Cell Activation, and Defective T-Regulatory Functions Promote Nephritis in Systemic Lupus Erythematosus |
title_full_unstemmed | Cytokine Overproduction, T-Cell Activation, and Defective T-Regulatory Functions Promote Nephritis in Systemic Lupus Erythematosus |
title_short | Cytokine Overproduction, T-Cell Activation, and Defective T-Regulatory Functions Promote Nephritis in Systemic Lupus Erythematosus |
title_sort | cytokine overproduction, t-cell activation, and defective t-regulatory functions promote nephritis in systemic lupus erythematosus |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910555/ https://www.ncbi.nlm.nih.gov/pubmed/20671931 http://dx.doi.org/10.1155/2010/457146 |
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