| pubmed-article:1712809 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1712809 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:1712809 | lifeskim:mentions | umls-concept:C0228174 | lld:lifeskim |
| pubmed-article:1712809 | lifeskim:mentions | umls-concept:C1257792 | lld:lifeskim |
| pubmed-article:1712809 | lifeskim:mentions | umls-concept:C0024348 | lld:lifeskim |
| pubmed-article:1712809 | lifeskim:mentions | umls-concept:C1533691 | lld:lifeskim |
| pubmed-article:1712809 | lifeskim:mentions | umls-concept:C1704419 | lld:lifeskim |
| pubmed-article:1712809 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
| pubmed-article:1712809 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:1712809 | pubmed:dateCreated | 1991-8-20 | lld:pubmed |
| pubmed-article:1712809 | pubmed:abstractText | Lysis of cerebral vascular endothelial cells (EC) by CD4-positive, myelin basic protein-specific encephalitogenic T cell lines was investigated. Unstimulated EC were not lysed, but culture in the presence of murine rIFN-gamma resulted in the expression of class II MHC (Ia) molecules and the concomitant ability to function as effective target cells for lysis. The possible requirement for Ia molecules was further demonstrated by antibody-blocking experiments. Lysis of EC targets also required the presence of specific Ag (myelin basic protein); PPD-specific T cell lines also lysed the PPD-pulsed EC. In all cases, lysis was directly proportional to E:T ratios. In addition, continuous passage of T cell lines resulted in the concomitant loss of encephalitogenicity and ability to affect EC lysis, indicating a possible relationship between these two factors. These results demonstrate that CD4+ T cells interact with cerebral vascular EC. It is suggested that such interactions may be important in the pathogenesis of diseases involving migrations of these cells across the blood-brain barrier. | lld:pubmed |
| pubmed-article:1712809 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1712809 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1712809 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:1712809 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1712809 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1712809 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1712809 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1712809 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:1712809 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:1712809 | pubmed:author | pubmed-author:SpatzMM | lld:pubmed |
| pubmed-article:1712809 | pubmed:author | pubmed-author:McCarronR MRM | lld:pubmed |
| pubmed-article:1712809 | pubmed:author | pubmed-author:McFarlinD EDE | lld:pubmed |
| pubmed-article:1712809 | pubmed:author | pubmed-author:RackeMM | lld:pubmed |
| pubmed-article:1712809 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1712809 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:1712809 | pubmed:volume | 147 | lld:pubmed |
| pubmed-article:1712809 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1712809 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1712809 | pubmed:pagination | 503-8 | lld:pubmed |
| pubmed-article:1712809 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:1712809 | pubmed:meshHeading | pubmed-meshheading:1712809-... | lld:pubmed |
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| pubmed-article:1712809 | pubmed:meshHeading | pubmed-meshheading:1712809-... | lld:pubmed |
| pubmed-article:1712809 | pubmed:meshHeading | pubmed-meshheading:1712809-... | lld:pubmed |
| pubmed-article:1712809 | pubmed:meshHeading | pubmed-meshheading:1712809-... | lld:pubmed |
| pubmed-article:1712809 | pubmed:meshHeading | pubmed-meshheading:1712809-... | lld:pubmed |
| pubmed-article:1712809 | pubmed:meshHeading | pubmed-meshheading:1712809-... | lld:pubmed |
| pubmed-article:1712809 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1712809 | pubmed:articleTitle | Cerebral vascular endothelial cells are effective targets for in vitro lysis by encephalitogenic T lymphocytes. | lld:pubmed |
| pubmed-article:1712809 | pubmed:affiliation | Laboratory of Neuropathology and Neuroanatomical Sciences, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD 20892. | lld:pubmed |
| pubmed-article:1712809 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1712809 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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