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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0003320,
umls-concept:C0019627,
umls-concept:C0021756,
umls-concept:C0037791,
umls-concept:C0085358,
umls-concept:C0205164,
umls-concept:C0443288,
umls-concept:C0591833,
umls-concept:C0678894,
umls-concept:C0719453,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1706438,
umls-concept:C2003905,
umls-concept:C2698600
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pubmed:issue |
10
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pubmed:dateCreated |
1993-11-12
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pubmed:abstractText |
The mechanism of antigen-specific suppression and reasons for aberrant major histocompatibility complex (MHC) class II restriction mediated by CD8+ T cells was investigated in a previously reported murine model of immunosuppression, generated by intraperitoneal priming with Mycobacterium vaccae. Both the CD4+ T helper cells (Th) and CD8+ T suppressor cell (Ts) of M. vaccae-primed mice recognized the 65-kDa antigen of the bacillus, presented by I-A and I-E, respectively. The CD8+ Ts could inhibit non-antigen-specific proliferation of primed CD4+ T cells induced by the exogenously added interleukin (IL)-2 (concanavalin A-stimulated culture supernatant). For inhibition, the Ts had to be activated by the 65-kDa antigen. The degree of inhibition was dependent upon the amount of added IL-2 and the relative numbers of primed CD8+ and CD4+ T cells. On incubation with antigen-presenting cells, and the 65-kDa antigen, the primed CD8+ T cells absorbed IL-2 as efficiently as primed CD4+ T cells. Based on this, it was concluded that the primed CD8+ T cells induced suppression by competition for IL-2. Employing the same model, the MHC restriction of recognition of the suppressor epitope of the 65-kDa antigen by the CD8+ Ts was investigated. The epitopes presented by diverse MHC class II molecules, such as self I-A, I-E and even allogeneic I-E were similar, because they were recognized by the same population of primed CD8+ Ts. Further, immunization of C57BL/6 mice with Ltk-cells expressing H-2 DkKk alloantigens, stimulated CD8+ T cells capable of recognizing M.vaccae 65-kDa antigen. Based on these data, it was proposed that recognition of the suppressor epitope of the 65-kDa antigen by the primed CD8+ Ts exhibits lack of restriction specificity imposed by MHC diversity.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Bacterial,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD8,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0014-2980
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2440-7
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8405043-Animals,
pubmed-meshheading:8405043-Antigens, Bacterial,
pubmed-meshheading:8405043-Antigens, CD8,
pubmed-meshheading:8405043-Histocompatibility Antigens Class I,
pubmed-meshheading:8405043-Histocompatibility Antigens Class II,
pubmed-meshheading:8405043-Interleukin-2,
pubmed-meshheading:8405043-Lymphocyte Activation,
pubmed-meshheading:8405043-Major Histocompatibility Complex,
pubmed-meshheading:8405043-Mice,
pubmed-meshheading:8405043-Mice, Inbred BALB C,
pubmed-meshheading:8405043-Mice, Inbred C3H,
pubmed-meshheading:8405043-Mice, Inbred C57BL,
pubmed-meshheading:8405043-Molecular Weight,
pubmed-meshheading:8405043-Mycobacterium,
pubmed-meshheading:8405043-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:8405043-T-Lymphocytes, Regulatory
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pubmed:year |
1993
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pubmed:articleTitle |
Murine CD8+ T suppressors against mycobacterial 65-kDa antigen compete for IL-2 and show lack of major histocompatibility complex-imposed restriction specificity in antigen recognition.
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pubmed:affiliation |
Department of Immunology, Haffkine Institute, Parel, Bombay, India.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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