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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
1987-1-29
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pubmed:abstractText |
We have used the murine model of spontaneous autoimmune interstitial nephritis in kdkd mice to examine the importance of abnormal immunoregulation in the expression of disease. T cells from naive congenic CBA/Ca mice suppress both histologic renal injury in the kdkd strain as well as the DTH reactivity to CBA/Ca renal tubular antigens mediated by lymphocytes from nephritic kdkd mice. These antigen-specific suppressor T cells are Lyt-2+, L3T4+, I-Jk+, genetically dominant and I-Jk restricted. Unfractionated spleen cells from young, prenephritic kdkd mice also demonstrate such suppressor function. Shortly preceding disease onset, however, net suppression is functionally bypassed by emergent contrasuppressor T cells. These regulatory cells are also Lyt-2+ and I-Jk+, and adhere both to the Vicia Villosa lectin and CBA/Ca TBM. By admixing these contrasuppressor cells with spleen cells from non-disease-prone CBA/Ca mice we were able to demonstrate the presence of DTH-reactive and nephritogenic effector cells in the latter population. Such nephritogenic effector cells could also be simply demonstrated after depletion of the suppressor cells with anti-I-Jk mAbs and complement. These findings support a role for contrasuppressor cells in the abrogation of tolerance to parenchymal self-antigens.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-2416810,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-2867113,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-3159824,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-376352,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-376701,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-50370,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-5098070,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6084403,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6152712,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6159417,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6195255,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6203971,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6205065,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6214163,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6224887,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6234375,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6242348,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6242848,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6384368,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6454751,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6454752,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6459945,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6459946,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6602021,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-677266,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6795302,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6801184,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-6975326,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-699062,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2947967-786519
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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 |
Jan
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pubmed:issn |
0022-1007
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
165
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
107-23
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:2947967-Age Factors,
pubmed-meshheading:2947967-Animals,
pubmed-meshheading:2947967-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:2947967-Antigens, Surface,
pubmed-meshheading:2947967-Autoimmune Diseases,
pubmed-meshheading:2947967-Basement Membrane,
pubmed-meshheading:2947967-Genes, Dominant,
pubmed-meshheading:2947967-Hypersensitivity, Delayed,
pubmed-meshheading:2947967-Immune Tolerance,
pubmed-meshheading:2947967-Immunity, Cellular,
pubmed-meshheading:2947967-Immunization, Passive,
pubmed-meshheading:2947967-Kidney Tubules,
pubmed-meshheading:2947967-Major Histocompatibility Complex,
pubmed-meshheading:2947967-Mice,
pubmed-meshheading:2947967-Mice, Mutant Strains,
pubmed-meshheading:2947967-Nephritis, Interstitial,
pubmed-meshheading:2947967-T-Lymphocytes,
pubmed-meshheading:2947967-T-Lymphocytes, Regulatory
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pubmed:year |
1987
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pubmed:articleTitle |
Contrasuppression in autoimmunity. Abnormal contrasuppression facilitates expression of nephritogenic effector T cells and interstitial nephritis in kdkd mice.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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