pubmed-article:6196206 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C0027651 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C0023418 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C0025918 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C0039195 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C1883178 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C0204727 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C0205419 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C0439851 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C0332325 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C0439806 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C0037791 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C1552596 | lld:lifeskim |
pubmed-article:6196206 | lifeskim:mentions | umls-concept:C1947931 | lld:lifeskim |
pubmed-article:6196206 | pubmed:issue | 11 | lld:pubmed |
pubmed-article:6196206 | pubmed:dateCreated | 1984-1-26 | lld:pubmed |
pubmed-article:6196206 | pubmed:abstractText | The AKR.H-2bSL1 tumor cell line is susceptible to H-2Kb-restricted cytotoxic T lymphocytes (CTL) directed against the subclass of AKR endogenous leukemia virus-induced tumors that express the Gross cell surface antigen (anti-AKR/Gross virus CTL). A variant subclone (cl.18-5) of AKR.H-2bSL1 was isolated, whose susceptibility to lysis by conventional or cloned lines of anti-AKR/Gross virus CTL was approximately 5% or less than that of the parental tumor. The cl.18-5 variant was also ineffective when used as an in vivo priming cell or an in vitro stimulator cell in the generation of anti-AKR/Gross virus CTL or as an unlabeled target cell in competitive inhibition assays. These results implied that the failure of cl.18-5 to be lysed was due to a lack of recognition by the CTL. In contrast, cl.18-5 was able to be lysed by and stimulate the generation of predominantly H-2Db-restricted CTL with apparent specificity for AKR minor histocompatibility antigens. The variant line was also about as susceptible as the parental AKR.H-2bSL1 line to both allogeneic CTL and to H-2Kb-restricted, TNP-specific CTL. Thus, the lack of recognition of cl.18-5 by anti-AKR/Gross virus CTL did not appear to be due to a failure to express functional H-2 products or to a generalized insusceptibility to H-2-restricted CTL. Rather, cl.18-5 appeared to be a selective variant and a useful probe for studying the specificity of anti-AKR/Gross virus CTL. | lld:pubmed |
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pubmed-article:6196206 | pubmed:language | eng | lld:pubmed |
pubmed-article:6196206 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:6196206 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:6196206 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:6196206 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:6196206 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:6196206 | pubmed:month | Nov | lld:pubmed |
pubmed-article:6196206 | pubmed:issn | 0014-2980 | lld:pubmed |
pubmed-article:6196206 | pubmed:author | pubmed-author:GreenW RWR | lld:pubmed |
pubmed-article:6196206 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:6196206 | pubmed:volume | 13 | lld:pubmed |
pubmed-article:6196206 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:6196206 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:6196206 | pubmed:pagination | 863-70 | lld:pubmed |
pubmed-article:6196206 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:6196206 | pubmed:year | 1983 | lld:pubmed |
pubmed-article:6196206 | pubmed:articleTitle | The specificity of H-2-restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus-induced tumors. I. Isolation of a selectively resistant variant tumor subclone. | lld:pubmed |
pubmed-article:6196206 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:6196206 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:6196206 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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