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rdf:type |
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lifeskim:mentions |
umls-concept:C0011616,
umls-concept:C0012463,
umls-concept:C0024518,
umls-concept:C0035820,
umls-concept:C0086574,
umls-concept:C0205147,
umls-concept:C0205263,
umls-concept:C0314603,
umls-concept:C0443288,
umls-concept:C1704410,
umls-concept:C2355612
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pubmed:issue |
3
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pubmed:dateCreated |
1978-5-17
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pubmed:abstractText |
Genetic restrictions governing the induction and expression of suppressor T cells (Ts) in tolerance to 1-fluoro-2,4-dinitrogenzene (DNFB) contract sensitivity were studied. Tolerance was induced by using 2,4-dinitrophenyl (DNP)-modified lymphoid cells (DNP-LC) as tolerogen. Two kinds of Ts were found-those produced by DNP-LC syngeneic to the donor of the Ts (syninduced Ts), and those produced by DNP-LC allogeneic to the donor of Ts (alloinduced Ts). Studies employing congenic resistant mouse strains indicated that recognition of DNP-modified-major histocompatibility region determinants on the tolerogenic DNP-LC was essential for the induction of both types of Ts. Non-H-2 genetic background was irrelevant to Ts induction. Mapping studies indicated that induction of both syninduced and alloinduced Ts was associated with recognition of DNP-modified-MHC region determinants which map to the right of the H-2G region (i.e., H-2D gene products). Tolerization of donor mice with DNP-LC which were H-2D region compatible, but not with H-2K or I region compatible DNP-LC, was both sufficient and required for the induction of hapten-specific syninduced Ts. Tolerization of donor mice with DNP-LC which were incompatible only at the H-2D region was sufficient for the induction of alloinduced Ts. These Ts were capable of suppressing recipient mice only if the recipients shared the H-2D region with the strain providing the DNP-LC tolerogen, and were not capable of suppressing recipients sharing all but the H-2D region with the tolerogen.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-1078737,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-1079849,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-1082137,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-1084899,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-1085311,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-1085340,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-1085418,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-1087316,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-1092799,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-129500,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-175126,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-299922,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-300292,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-300774,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-301091,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-302178,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-4109878,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-4154454,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-4267208,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-4279271,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-4547338,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-47901,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-874323,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-874422,
http://linkedlifedata.com/resource/pubmed/commentcorrection/305458-915281
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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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 |
147
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
788-99
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:305458-Animals,
pubmed-meshheading:305458-Chromosome Mapping,
pubmed-meshheading:305458-Dermatitis, Contact,
pubmed-meshheading:305458-Dinitrobenzenes,
pubmed-meshheading:305458-Dinitrofluorobenzene,
pubmed-meshheading:305458-H-2 Antigens,
pubmed-meshheading:305458-Haptens,
pubmed-meshheading:305458-Immune Tolerance,
pubmed-meshheading:305458-Immunity, Cellular,
pubmed-meshheading:305458-Immunosuppression,
pubmed-meshheading:305458-Mice,
pubmed-meshheading:305458-Nitrobenzenes,
pubmed-meshheading:305458-T-Lymphocytes
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pubmed:year |
1978
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pubmed:articleTitle |
Genetic restrictions for the induction of suppressor T cells by hapten-modified lymphoid cells in tolerance to 1-fluoro-2,4-dinitrobenzene contact sensitivity. Role of the H-2D region of the major histocompatibility complex.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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