| pubmed-article:6223093 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:6223093 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
| pubmed-article:6223093 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:6223093 | lifeskim:mentions | umls-concept:C0032659 | lld:lifeskim |
| pubmed-article:6223093 | lifeskim:mentions | umls-concept:C0024141 | lld:lifeskim |
| pubmed-article:6223093 | lifeskim:mentions | umls-concept:C0007613 | lld:lifeskim |
| pubmed-article:6223093 | lifeskim:mentions | umls-concept:C0038856 | lld:lifeskim |
| pubmed-article:6223093 | lifeskim:mentions | umls-concept:C1457869 | lld:lifeskim |
| pubmed-article:6223093 | lifeskim:mentions | umls-concept:C1709305 | lld:lifeskim |
| pubmed-article:6223093 | lifeskim:mentions | umls-concept:C2003905 | lld:lifeskim |
| pubmed-article:6223093 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:6223093 | pubmed:dateCreated | 1983-8-26 | lld:pubmed |
| pubmed-article:6223093 | pubmed:abstractText | The autologous mixed lymphocyte reaction (MLR) is thought to be part of a regulatory role of T cells on B cell function. OKT4+, but not OKT8+, cells can proliferate in response to autologous non-T cells. Moreover, the OKT4+ cell population activated early in the course of autologous MLR functioned as inducer cells for the differentiation of B cells, whereas later in the response, the activated OKT4+ cells were particularly enriched in suppressor cells. A part of the autologous MLR appears to be an important pathway for the activation of feedback suppression mechanisms among cells contained within the OKT4+ populations. Patients with systemic lupus erythematosus (SLE) were studied with regard to the following OKT4+ cell functions in vitro after activation in the autologous MLR: a) proliferative response, and b) helper and suppressor activities for differentiation of B cells. A marked reduction in the proliferative response of OKT4+ cells was observed in SLE patients. SLE OKT4+ cells activated in the autologous MLR could function as helper cells but could not exert any suppressor activity. This OKT4+ cell abnormality was present regardless of the disease activity, and occurred in the absence of autoantibodies including anti-T cell antibodies. Instead, SLE anti-T cell antibodies could preferentially eliminate cells bearing the OKT8+ phenotype characteristic of suppressor cells in populations of normal T cells. These results suggest that the defect in the suppressor circuits among OKT4+ cell populations is intrinsic to SLE lymphocytes and that the OKT8+ suppressor T cell defect is caused by antibodies produced by the B cells of SLE patients. | lld:pubmed |
| pubmed-article:6223093 | pubmed:language | eng | lld:pubmed |
| pubmed-article:6223093 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:6223093 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:6223093 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:6223093 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:6223093 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:6223093 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:6223093 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:6223093 | pubmed:author | pubmed-author:UedaYY | lld:pubmed |
| pubmed-article:6223093 | pubmed:author | pubmed-author:TakadaSS | lld:pubmed |
| pubmed-article:6223093 | pubmed:author | pubmed-author:KotaniHH | lld:pubmed |
| pubmed-article:6223093 | pubmed:author | pubmed-author:SakaneTT | lld:pubmed |
| pubmed-article:6223093 | pubmed:author | pubmed-author:MurakawaYY | lld:pubmed |
| pubmed-article:6223093 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:6223093 | pubmed:volume | 131 | lld:pubmed |
| pubmed-article:6223093 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:6223093 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:6223093 | pubmed:pagination | 753-61 | lld:pubmed |
| pubmed-article:6223093 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:6223093 | pubmed:meshHeading | pubmed-meshheading:6223093-... | lld:pubmed |
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| pubmed-article:6223093 | pubmed:meshHeading | pubmed-meshheading:6223093-... | lld:pubmed |
| pubmed-article:6223093 | pubmed:meshHeading | pubmed-meshheading:6223093-... | lld:pubmed |
| pubmed-article:6223093 | pubmed:meshHeading | pubmed-meshheading:6223093-... | lld:pubmed |
| pubmed-article:6223093 | pubmed:meshHeading | pubmed-meshheading:6223093-... | lld:pubmed |
| pubmed-article:6223093 | pubmed:meshHeading | pubmed-meshheading:6223093-... | lld:pubmed |
| pubmed-article:6223093 | pubmed:year | 1983 | lld:pubmed |
| pubmed-article:6223093 | pubmed:articleTitle | A defect in the suppressor circuits among OKT4+ cell populations in patients with systemic lupus erythematosus occurs independently of a defect in the OKT8+ suppressor T cell function. | lld:pubmed |
| pubmed-article:6223093 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:6223093 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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