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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1989-9-1
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pubmed:abstractText |
A new model of experimental glomerulonephritis (GN) in which a cell-mediated (delayed-type) reaction predominated was established. Cationized TNP-BSA conjugates were planted in the kidney of rats by perfusion via the renal artery. Rats which had been sensitized with the TNP hapten 7 days previously revealed marked exudative and proliferative changes in their glomeruli, accompanied by transient proteinuria. A cellular influx was seen without deposition of any autologous antibody. The resulting data are compatible with the idea that cell-mediated immune reactions can participate in tissue damage in glomerular disease.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-146726,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-2464447,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-2859686,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-4160044,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-4193072,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-4540732,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-6224427,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-6225823,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-6238207,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-6343545,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-6460074,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-6585368,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-6766974,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-6969776,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-7041510,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-7245332,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2473861-78959
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0009-9104
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
76
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
463-8
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:2473861-Animals,
pubmed-meshheading:2473861-Antibody Formation,
pubmed-meshheading:2473861-Dermatitis, Contact,
pubmed-meshheading:2473861-Epitopes,
pubmed-meshheading:2473861-Glomerulonephritis,
pubmed-meshheading:2473861-Haptens,
pubmed-meshheading:2473861-Hypersensitivity, Delayed,
pubmed-meshheading:2473861-Male,
pubmed-meshheading:2473861-Proteinuria,
pubmed-meshheading:2473861-Rats,
pubmed-meshheading:2473861-Rats, Inbred Strains,
pubmed-meshheading:2473861-Serum Albumin, Bovine,
pubmed-meshheading:2473861-Trinitrobenzenes
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pubmed:year |
1989
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pubmed:articleTitle |
Hapten-specific cellular immune response producing glomerular injury.
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pubmed:affiliation |
Department of Immunology, Niigata University School of Medicine, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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