Mediators of Inflammation and Their Effect on Resident Renal Cells: Implications in Lupus Nephritis
Lupus nephritis affects up to 70% of patients with systemic lupus erythematosus and is a major cause of morbidity and mortality. It is characterized by a breakdown of immune tolerance, production of autoantibodies, and deposition of immune complexes within the kidney parenchyma, resulting in local i...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Clinical and Developmental Immunology |
| Online Access: | http://dx.doi.org/10.1155/2013/317682 |
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| _version_ | 1832558329137725440 |
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| author | Susan Yung Kwok Fan Cheung Qing Zhang Tak Mao Chan |
| author_facet | Susan Yung Kwok Fan Cheung Qing Zhang Tak Mao Chan |
| author_sort | Susan Yung |
| collection | DOAJ |
| description | Lupus nephritis affects up to 70% of patients with systemic lupus erythematosus and is a major cause of morbidity and mortality. It is characterized by a breakdown of immune tolerance, production of autoantibodies, and deposition of immune complexes within the kidney parenchyma, resulting in local inflammation and subsequent organ damage. To date, numerous mediators of inflammation have been implicated in the development and progression of lupus nephritis, and these include cytokines, chemokines, and glycosaminoglycans. Of these, type I interferons (IFNs) can increase both gene and protein expression of cytokines and chemokines associated with lupus susceptibility, and interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and hyaluronan have been shown to elicit both pro- and anti-inflammatory effects on infiltrating and resident renal cells depending on the status of their microenvironment. Expression of IL-6, TNF-α, type I IFNs, and hyaluronan are increased in the kidneys of patients and mice with active lupus nephritis and have been shown to contribute to disease pathogenesis. There is also evidence that despite clinical remission, ongoing inflammatory processes may occur within the glomerular and tubulointerstitial compartments of the kidney, which further promote kidney injury. In this review, we provide an overview of the synthesis and putative roles of IL-6, TNF-α, IFN-α, and hyaluronan in the pathogenesis of lupus nephritis focusing on their effects on human mesangial cells and proximal renal tubular epithelial cells. |
| format | Article |
| id | doaj-art-900919be447447edb5d8ec232f061de0 |
| institution | Kabale University |
| issn | 1740-2522 1740-2530 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Clinical and Developmental Immunology |
| spelling | doaj-art-900919be447447edb5d8ec232f061de02025-02-03T01:32:45ZengWileyClinical and Developmental Immunology1740-25221740-25302013-01-01201310.1155/2013/317682317682Mediators of Inflammation and Their Effect on Resident Renal Cells: Implications in Lupus NephritisSusan Yung0Kwok Fan Cheung1Qing Zhang2Tak Mao Chan3Department of Medicine, The University of Hong Kong, Hong KongDepartment of Medicine, The University of Hong Kong, Hong KongDepartment of Medicine, The University of Hong Kong, Hong KongDepartment of Medicine, The University of Hong Kong, Hong KongLupus nephritis affects up to 70% of patients with systemic lupus erythematosus and is a major cause of morbidity and mortality. It is characterized by a breakdown of immune tolerance, production of autoantibodies, and deposition of immune complexes within the kidney parenchyma, resulting in local inflammation and subsequent organ damage. To date, numerous mediators of inflammation have been implicated in the development and progression of lupus nephritis, and these include cytokines, chemokines, and glycosaminoglycans. Of these, type I interferons (IFNs) can increase both gene and protein expression of cytokines and chemokines associated with lupus susceptibility, and interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and hyaluronan have been shown to elicit both pro- and anti-inflammatory effects on infiltrating and resident renal cells depending on the status of their microenvironment. Expression of IL-6, TNF-α, type I IFNs, and hyaluronan are increased in the kidneys of patients and mice with active lupus nephritis and have been shown to contribute to disease pathogenesis. There is also evidence that despite clinical remission, ongoing inflammatory processes may occur within the glomerular and tubulointerstitial compartments of the kidney, which further promote kidney injury. In this review, we provide an overview of the synthesis and putative roles of IL-6, TNF-α, IFN-α, and hyaluronan in the pathogenesis of lupus nephritis focusing on their effects on human mesangial cells and proximal renal tubular epithelial cells.http://dx.doi.org/10.1155/2013/317682 |
| spellingShingle | Susan Yung Kwok Fan Cheung Qing Zhang Tak Mao Chan Mediators of Inflammation and Their Effect on Resident Renal Cells: Implications in Lupus Nephritis Clinical and Developmental Immunology |
| title | Mediators of Inflammation and Their Effect on Resident Renal Cells: Implications in Lupus Nephritis |
| title_full | Mediators of Inflammation and Their Effect on Resident Renal Cells: Implications in Lupus Nephritis |
| title_fullStr | Mediators of Inflammation and Their Effect on Resident Renal Cells: Implications in Lupus Nephritis |
| title_full_unstemmed | Mediators of Inflammation and Their Effect on Resident Renal Cells: Implications in Lupus Nephritis |
| title_short | Mediators of Inflammation and Their Effect on Resident Renal Cells: Implications in Lupus Nephritis |
| title_sort | mediators of inflammation and their effect on resident renal cells implications in lupus nephritis |
| url | http://dx.doi.org/10.1155/2013/317682 |
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