Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1989-5-31
pubmed:abstractText
The pathogenesis of SLE is commonly attributed to the deposition of circulating immune complexes consisting of DNA and anti-DNA autoantibodies. However, recent work has shown multiple cross-reactions between anti-DNA antibodies and a variety of cellular and extracellular Ag. To test the possibility that these antibodies interact directly with glomerular Ag and induce kidney dysfunction, we applied mouse and human anti-DNA IgG to the isolated perfused rat kidney. The NZB/NZW mouse monoclonal anti-DNA bound to glomerular Ag with a concomitant induction of proteinuria and a decrease in inulin clearance. The albumin excretion was 2301 +/- 734 micrograms/min at 160 min of perfusion, as compared with 85 +/- 21 micrograms/min in controls (p less than 0.001). The inulin clearance was reduced to 0.17 +/- 0.02 ml/min as compared with 0.28 +/- 0.09 ml/min in controls (p less than 0.05). Polyclonal anti-DNA IgG obtained from patients with lupus nephritis bound to rat glomeruli and induced albumin excretion of 542 +/- 217 micrograms/min at 160 min of perfusion, as compared with 163 +/- 77 micrograms/min in controls (p = NS). The addition of plasma as a source of C to the human IgG increased the proteinuria markedly (albumin excretion of 1115 +/- 195 micrograms/min at 160 min of perfusion, p less than 0.02), probably due to C activation. Preincubation of the reactive mouse and human IgG with DNA completely abolished their binding to renal tissue and its physiologic consequences. These results suggest that direct binding of anti-DNA antibodies to renal Ag may play an important role in the induction of lupus nephritis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
142
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3076-82
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:2785132-Adolescent, pubmed-meshheading:2785132-Adult, pubmed-meshheading:2785132-Animals, pubmed-meshheading:2785132-Antibodies, Antinuclear, pubmed-meshheading:2785132-Autoantigens, pubmed-meshheading:2785132-Binding Sites, Antibody, pubmed-meshheading:2785132-Complement System Proteins, pubmed-meshheading:2785132-DNA, pubmed-meshheading:2785132-Female, pubmed-meshheading:2785132-Humans, pubmed-meshheading:2785132-Immunoglobulin G, pubmed-meshheading:2785132-Kidney, pubmed-meshheading:2785132-Lupus Erythematosus, Systemic, pubmed-meshheading:2785132-Male, pubmed-meshheading:2785132-Mice, pubmed-meshheading:2785132-Mice, Inbred BALB C, pubmed-meshheading:2785132-Middle Aged, pubmed-meshheading:2785132-Perfusion, pubmed-meshheading:2785132-Plasma, pubmed-meshheading:2785132-Rats, pubmed-meshheading:2785132-Rats, Inbred Strains
pubmed:year
1989
pubmed:articleTitle
Anti-DNA antibodies bind directly to renal antigens and induce kidney dysfunction in the isolated perfused rat kidney.
pubmed:affiliation
Department of Medicine, Hadassah University Hospitals, Jerusalem, Israel.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't