pubmed-article:6226679 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:6226679 | lifeskim:mentions | umls-concept:C0684336 | lld:lifeskim |
pubmed-article:6226679 | lifeskim:mentions | umls-concept:C0011615 | lld:lifeskim |
pubmed-article:6226679 | lifeskim:mentions | umls-concept:C0439859 | lld:lifeskim |
pubmed-article:6226679 | lifeskim:mentions | umls-concept:C0023509 | lld:lifeskim |
pubmed-article:6226679 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:6226679 | pubmed:dateCreated | 1983-12-17 | lld:pubmed |
pubmed-article:6226679 | pubmed:abstractText | The T cell proliferative response to autologous non-T cells is termed the autologous mixed lymphocyte reaction (AMLR). Recent studies have suggested that the AMLR represents an inducer circuit for the activation of T8+ suppressor/cytotoxic effector cells. Since atopic dermatitis (AD) patients are deficient in T8+ cytolytic T cell function, we investigated the AMLR in AD. When sheep erythrocytes were used to separate T cells from non-T cells, the AMLR was found to be significantly decreased (P less than 0.001) in AD patients (n = 11; delta cpm = 1,550 +/- 393) when compared with normal control subjects (n = 13; delta cpm = 25,819 +/- 4,609). To exclude the possibility that these results were an artifact of the sheep erythrocyte separation, T cells were also separated on a fluorescence-activated cell sorter after treatment of peripheral blood lymphocytes with the OKT3 monoclonal antibody. AD T cells separated by the latter method were also found to have a significantly reduced AMLR response when compared with similarly treated normal T cells. Co-culture studies using cells from AD patients and their HLA identical siblings indicated that the defect resided at the responder T cell level rather than at the stimulator non-T cell level. Co-culture studies revealed no evidence for excessive suppressor cell activity resulting in the decreased AMLR. However, enumeration of T cells reactive with the monoclonal antibody T29, which recognizes a subset of T cells proliferating in the AMLR, demonstrated that AD patients (n = 8; % T29 = 2.5 +/- 0.7) had a significantly decreased (P less than 0.001) number of circulating T29+ T cells when compared with normal controls (n = 8; % T29 = 10.4 +/- 0.8). These studies suggest that a deficiency of T4+ T29+ cells contributes to the deficient AMLR in AD and possibly underlies the abnormalities of T8+ effector cells present in this disease. | lld:pubmed |
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pubmed-article:6226679 | pubmed:language | eng | lld:pubmed |
pubmed-article:6226679 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:6226679 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:6226679 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:6226679 | pubmed:month | Oct | lld:pubmed |
pubmed-article:6226679 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:6226679 | pubmed:author | pubmed-author:GehaR SRS | lld:pubmed |
pubmed-article:6226679 | pubmed:author | pubmed-author:FrankelRR | lld:pubmed |
pubmed-article:6226679 | pubmed:author | pubmed-author:LeungD YDY | lld:pubmed |
pubmed-article:6226679 | pubmed:author | pubmed-author:SaryanJ AJA | lld:pubmed |
pubmed-article:6226679 | pubmed:author | pubmed-author:LareauMM | lld:pubmed |
pubmed-article:6226679 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:6226679 | pubmed:volume | 72 | lld:pubmed |
pubmed-article:6226679 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:6226679 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:6226679 | pubmed:pagination | 1482-6 | lld:pubmed |
pubmed-article:6226679 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:6226679 | pubmed:year | 1983 | lld:pubmed |
pubmed-article:6226679 | pubmed:articleTitle | Impairment of the autologous mixed lymphocyte reaction in atopic dermatitis. | lld:pubmed |
pubmed-article:6226679 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:6226679 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:6226679 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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