pubmed-article:1968084 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1968084 | lifeskim:mentions | umls-concept:C1332717 | lld:lifeskim |
pubmed-article:1968084 | lifeskim:mentions | umls-concept:C1706438 | lld:lifeskim |
pubmed-article:1968084 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:1968084 | lifeskim:mentions | umls-concept:C0085358 | lld:lifeskim |
pubmed-article:1968084 | lifeskim:mentions | umls-concept:C1413244 | lld:lifeskim |
pubmed-article:1968084 | lifeskim:mentions | umls-concept:C2698600 | lld:lifeskim |
pubmed-article:1968084 | lifeskim:mentions | umls-concept:C2347644 | lld:lifeskim |
pubmed-article:1968084 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
pubmed-article:1968084 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
pubmed-article:1968084 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
pubmed-article:1968084 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
pubmed-article:1968084 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:1968084 | pubmed:dateCreated | 1990-3-16 | lld:pubmed |
pubmed-article:1968084 | pubmed:abstractText | Interactions between self-MHC molecules and T cells are necessary for the proper development of mature T cells, in part due to an absolute requirement for self-MHC-TCR interactions. Recently, we showed that CD4-mediated interactions also participate in shaping the T cell repertoire during thymic maturation. We now examine the possible role of the CD8 molecule during in vivo T cell development. Our results demonstrate that perinatal thymi treated with intact anti-CD8 mAb fail to generate CD8 single-positive T cells, while the generation of the other main phenotypes remains unchanged. Most importantly, the use of F(ab')2 anti-CD8 mAb fragments gave identical results, i.e., lack of generation of CD4-/CD8+ cells, with no effect on the generation of CD4+/CD8+. Furthermore, selective blocking of one CD8 allele with F(ab')2 mAbs in F1 mice expressing both CD8 alleles did not interfere with the development of CD4-/CD8+ cells, demonstrating that the absence of CD8+ T cells in homozygous mice is not due to depletion, but rather is caused by a lack of positive selection. This is most likely attributable to a deficient CD8-MHC class I interaction. Our findings strongly advocate that CD8 molecules are vital to the selection process that leads to the development of mature single-positive CD8 T cells. | lld:pubmed |
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pubmed-article:1968084 | pubmed:language | eng | lld:pubmed |
pubmed-article:1968084 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1968084 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:1968084 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1968084 | pubmed:month | Feb | lld:pubmed |
pubmed-article:1968084 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:1968084 | pubmed:author | pubmed-author:JonesL ALA | lld:pubmed |
pubmed-article:1968084 | pubmed:author | pubmed-author:LongoD LDL | lld:pubmed |
pubmed-article:1968084 | pubmed:author | pubmed-author:KruisbeekA... | lld:pubmed |
pubmed-article:1968084 | pubmed:author | pubmed-author:Zúñiga-Pflück... | lld:pubmed |
pubmed-article:1968084 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1968084 | pubmed:day | 1 | lld:pubmed |
pubmed-article:1968084 | pubmed:volume | 171 | lld:pubmed |
pubmed-article:1968084 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1968084 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1968084 | pubmed:pagination | 427-37 | lld:pubmed |
pubmed-article:1968084 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:1968084 | pubmed:year | 1990 | lld:pubmed |
pubmed-article:1968084 | pubmed:articleTitle | CD8 is required during positive selection of CD4-/CD8+ T cells. | lld:pubmed |
pubmed-article:1968084 | pubmed:affiliation | Biological Response Modifiers Program, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. | lld:pubmed |
pubmed-article:1968084 | pubmed:publicationType | Journal Article | lld:pubmed |
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