| pubmed-article:2840801 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2840801 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
| pubmed-article:2840801 | lifeskim:mentions | umls-concept:C0022686 | lld:lifeskim |
| pubmed-article:2840801 | lifeskim:mentions | umls-concept:C0149678 | lld:lifeskim |
| pubmed-article:2840801 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:2840801 | lifeskim:mentions | umls-concept:C0205177 | lld:lifeskim |
| pubmed-article:2840801 | lifeskim:mentions | umls-concept:C0205191 | lld:lifeskim |
| pubmed-article:2840801 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:2840801 | pubmed:dateCreated | 1988-9-1 | lld:pubmed |
| pubmed-article:2840801 | pubmed:abstractText | Natural killer (NK) cell activity, lymphokine activated killer (LAK) activity and Epstein-Barr virus specific cytotoxic T lymphocyte (EBV-CTL) activity were examined in 10 children with chronic active EB-virus infection and an adult with persistently positive early antigen-antibody to EB-virus. NK cell activity against erythroleukemia cell line K-562 was significantly (p less than 0.005) lower in the patients (22.3 +/- 8.5%, mean +/- SD) than in normal controls (40.4 +/- 15.9%). Spontaneous cytotoxicity against an EB-virus transformed autologous lymphoblastoid cell line was 15.0 +/- 7.6% in the patients, and was comparable to spontaneous cytotoxicity activity in normal controls (11.7 +/- 4.3%). LAK activity against Raji cells was significantly (p less than 0.02) lower in the patients (14.6 +/- 11.4%) than in normal controls (29.2 +/- 15.9%). EBV-CTL activity against an EB-virus transformed autologous lymphoblastoid cell line was significantly (p less than 0.005) lower in the patients (11.8 +/- 5.5%) than in seropositive normal controls (33.7 +/- 14.7%). No regression of the lymphoblastoid cell line was observed when EBV-CTL activity of the patients was tested by regression assay. It is conceivable that defects in both EB-virus specific and nonspecific killer cell activities play important roles in the pathogenetic abnormalities which allow EB-virus infection to progress to a chronic active state. | lld:pubmed |
| pubmed-article:2840801 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2840801 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2840801 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:2840801 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2840801 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2840801 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:2840801 | pubmed:issn | 0386-300X | lld:pubmed |
| pubmed-article:2840801 | pubmed:author | pubmed-author:MatsumotoKK | lld:pubmed |
| pubmed-article:2840801 | pubmed:author | pubmed-author:OharaYY | lld:pubmed |
| pubmed-article:2840801 | pubmed:author | pubmed-author:KurashigeTT | lld:pubmed |
| pubmed-article:2840801 | pubmed:author | pubmed-author:FujiedaMM | lld:pubmed |
| pubmed-article:2840801 | pubmed:author | pubmed-author:WakiguchiHH | lld:pubmed |
| pubmed-article:2840801 | pubmed:author | pubmed-author:WakiguchiAA | lld:pubmed |
| pubmed-article:2840801 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2840801 | pubmed:volume | 42 | lld:pubmed |
| pubmed-article:2840801 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2840801 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2840801 | pubmed:pagination | 137-42 | lld:pubmed |
| pubmed-article:2840801 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:meshHeading | pubmed-meshheading:2840801-... | lld:pubmed |
| pubmed-article:2840801 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:2840801 | pubmed:articleTitle | Defective killer cell activity in patients with chronic active Epstein-Barr virus infection. | lld:pubmed |
| pubmed-article:2840801 | pubmed:affiliation | Department of Pediatrics, Kochi Medical School, Japan. | lld:pubmed |
| pubmed-article:2840801 | pubmed:publicationType | Journal Article | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:2840801 | lld:pubmed |
