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Pathogenesis of kidney disease in systemic lupus erythematosus
Current Opinion in Rheumatology, 08/18/09
Bagavant H et al. - Lupus glomerulonephritis is a prototype of immune complex disease mediated by autoantibodies of multiple specificities, one of which is anti-DNA. In addition to systemic autoimmunity, end-organ responses, and end-organ resistance to damage are also critical in determining disease outcome. This understanding might facilitate in the design of novel therapeutic approaches for systemic lupus erythematosus (SLE).
Methods- Review to discuss recent literature on pathogenetic mechanisms of lupus glomerulonephritis
- Characteristic features of lupus glomerulonephritis:
- Glomerular immune complexes AND
- Autoantibodies of multiple specificities
- participate in the formation of immune complexes, deposited in the kidneys
- Renal infiltration by T cells,
- macrophages, and dendritic cells
- have a dominant role in the progression, leading to renal failure
- Activation of Toll-like receptors modulates autoantibody production and systemic interferon responses
- However, glomerular cell responses to immune injury influence disease outcome
- participate in the formation of immune complexes, deposited in the kidneys
- New insights on the genetics of susceptibility to end-organ damage:
- Gene expression profiles during disease progression provide potential markers for diagnosis of lupus glomerulonephritis progression and flares
- Studies of end-organ responses provide new targets for therapeutic interventions
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