Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1985-8-9
pubmed:abstractText
The human Epstein-Barr virus transformed lymphoblastoid cell line (EBV-LCL) 721 and MHC haplotype loss variants derived from it were utilized to dissect the functional role of MHC genes in the proliferative response of autologous T lymphocytes to EBV-LCL. LCL-721 is heterozygous at all phenotypically defined MHC loci. One type of LCL-721 variant expresses only determinants encoded by the maternal (m) haplotype and the other expresses determinants encoded by the paternal (p) haplotype. Autologous (individual A) primary proliferative responses are strong to each type of haplotype deletant. The strong tertiary responses to the priming haplotype in comparison to the relatively weak responses to the reciprocal haplotype indicate that MHC linked genes encoded by each haplotype are important in the autologous response to EBV-LCL. Similar specific tertiary responses are observed when peripheral blood lymphocytes (PBLs) from the donor's mother are used as responding cells. Allogeneic responses were also studied by priming PBLs from unrelated donors with the haplotype deletants. Quantitative comparisons of the proliferation by primed allogeneic and autologous lymphocytes stimulated by irradiated PBLs from donor A and her mother, and by LCL-721 and its variants, show that some of the tertiary responses involve specific recognition of EBV-LCL while others detect recognition of alloantigens.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0198-8859
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
177-91
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1985
pubmed:articleTitle
The proliferative immune response to autologous Epstein-Barr virus-transformed lymphoblastoid cells. I. Studies with HLA haplotype loss variants demonstrate a role for MHC-linked genes.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't