Document Detail


Pathogenesis of kidney disease in systemic lupus erythematosus.
MedLine Citation:
PMID:  19584729     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE OF REVIEW: A combination of systemic autoimmunity and tissue response to immune injury underlie renal involvement in lupus erythematosus. In this review, we discuss recent literature investigating pathogenetic mechanisms of lupus glomerulonephritis.
RECENT FINDINGS: In lupus glomerulonephritis, glomerular immune complexes were believed to be the primary mediators of renal disease. Recent studies make it apparent that 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 of lupus glomerulonephritis 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. In addition, new insights on the genetics of susceptibility to end-organ damage in lupus glomerulonephritis have been discovered. Differential glomerular responses reflected in gene expression profiles during disease progression provide potential markers for diagnosis of lupus glomerulonephritis progression and flares. In addition, studies of end-organ responses provide new targets for therapeutic interventions.
SUMMARY: Lupus glomerulonephritis is a prototype of immune complex disease mediated by autoantibodies of multiple specificities, one of which is anti-DNA. Murine models of spontaneous systemic lupus erythematosus have been critical for understanding the underlying disease. Recent studies demonstrate that in addition to systemic autoimmunity, end-organ responses, and end-organ resistance to damage are also critical in determining disease outcome. This understanding should influence design of novel therapeutic approaches in systemic lupus erythematosus.
Authors:
Harini Bagavant; Shu Man Fu
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current opinion in rheumatology     Volume:  21     ISSN:  1531-6963     ISO Abbreviation:  Curr Opin Rheumatol     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-08-13     Completed Date:  2009-11-04     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  9000851     Medline TA:  Curr Opin Rheumatol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  489-94     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies, Antinuclear / metabolism
Autoantibodies / metabolism
Autoimmunity
Genetic Predisposition to Disease
Humans
Lupus Erythematosus, Systemic / complications*,  genetics,  immunology
Lupus Nephritis / etiology*,  genetics,  immunology
Mice
Signal Transduction / immunology
T-Lymphocytes / immunology
Grant Support
ID/Acronym/Agency:
P50-AR045222/AR/NIAMS NIH HHS; R01 DK069769/DK/NIDDK NIH HHS; R01 DK069769/DK/NIDDK NIH HHS; R01 DK069769-04/DK/NIDDK NIH HHS; R01-AR047988/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/Antibodies, Antinuclear; 0/Autoantibodies
Comments/Corrections

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