Lupus Nephritis: An Overview of Recent Findings
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...
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| Format: | Online |
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Hindawi Publishing Corporation
2012
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3318208/ |
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pubmed-33182082012-04-25 Lupus Nephritis: An Overview of Recent Findings de Zubiria Salgado, Alberto Herrera-Diaz, Catalina Review Article 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. Hindawi Publishing Corporation 2012 2012-03-22 /pmc/articles/PMC3318208/ /pubmed/22536486 http://dx.doi.org/10.1155/2012/849684 Text en Copyright © 2012 A. de Zubiria Salgado and C. Herrera-Diaz. https://creativecommons.org/licenses/by/3.0/ 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. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
de Zubiria Salgado, Alberto Herrera-Diaz, Catalina |
| spellingShingle |
de Zubiria Salgado, Alberto Herrera-Diaz, Catalina Lupus Nephritis: An Overview of Recent Findings |
| author_facet |
de Zubiria Salgado, Alberto Herrera-Diaz, Catalina |
| author_sort |
de Zubiria Salgado, Alberto |
| title |
Lupus Nephritis: An Overview of Recent Findings |
| title_short |
Lupus Nephritis: An Overview of Recent Findings |
| title_full |
Lupus Nephritis: An Overview of Recent Findings |
| title_fullStr |
Lupus Nephritis: An Overview of Recent Findings |
| title_full_unstemmed |
Lupus Nephritis: An Overview of Recent Findings |
| title_sort |
lupus nephritis: an overview of recent findings |
| description |
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. |
| publisher |
Hindawi Publishing Corporation |
| publishDate |
2012 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3318208/ |
| _version_ |
1611518817547059200 |