Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1992-7-10
pubmed:abstractText
To determine the relative ability of allogeneic endothelial cells to stimulate helper T lymphocytes (HTL), human PBMC or purified T cells were incubated in conventional lymphocyte microcultures or in limiting dilution microcultures with allogeneic human umbilical vein endothelia (HUVE), with cytokine-treated allogeneic HUVE, or with allogeneic peripheral blood monocytes. These cultures were tested for IL-2 production as an index of HTL stimulation. Dose-response studies in conventional lymphocyte cultures indicated that allogeneic monocytes were better than allogeneic HUVE at stimulating IL-2 production. Limiting dilution analyses revealed that untreated HUVE and TNF-treated HUVE stimulated small numbers of HTL (approximately 1 HTL/30,000 PBMC), whereas 5 to 10 times more HTL were stimulated by IFN-gamma-treated HUVE and 10 to 20 times more HTL were stimulated by allogeneic monocytes. Serologic deletion studies revealed that most of the high frequency HTL responding to IFN-gamma-treated HUVE were CD4+, whereas most of the low frequency HTL responding to nontreated HUVE or to TNF-treated HUVE were CD8+. Interestingly, mAb to MHC class I and class II molecules, which significantly impaired HUVE-induced proliferation, caused little interference with HUVE-induced IL-2 production. Finally, polymerase chain reaction analysis demonstrated that untreated allogeneic HUVE cells could stimulate PBMC to produce mRNA for IFN-gamma, as well as for IL-2. These data demonstrate the following hierarchy of allogeneic stimulatory capacity for human HTL: monocytes greater than IFN-gamma-treated HUVE much greater than TNF-treated HUVE = nontreated HUVE. Further, these data suggest that non-activated allogeneic endothelial cells can initiate immune responses by inducing IL-2 and IFN-gamma. Because IFN-gamma can induce MHC class II expression by the endothelial cells, this could recruit large numbers of CD4+ T cells for IL-2 production.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
148
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3753-60
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:1351087-Antigens, CD3, pubmed-meshheading:1351087-Antigens, CD8, pubmed-meshheading:1351087-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:1351087-CD4-Positive T-Lymphocytes, pubmed-meshheading:1351087-Cells, Cultured, pubmed-meshheading:1351087-Cytokines, pubmed-meshheading:1351087-Endothelium, Vascular, pubmed-meshheading:1351087-HLA-D Antigens, pubmed-meshheading:1351087-Histocompatibility Antigens Class I, pubmed-meshheading:1351087-Humans, pubmed-meshheading:1351087-Interferon-gamma, pubmed-meshheading:1351087-Interleukin-2, pubmed-meshheading:1351087-Lymphocyte Activation, pubmed-meshheading:1351087-Receptors, Antigen, T-Cell, pubmed-meshheading:1351087-T-Lymphocyte Subsets, pubmed-meshheading:1351087-T-Lymphocytes, Helper-Inducer, pubmed-meshheading:1351087-Tumor Necrosis Factor-alpha
pubmed:year
1992
pubmed:articleTitle
Alloantigenicity of human endothelial cells. 1. Frequency and phenotype of human T helper lymphocytes that can react to allogeneic endothelial cells.
pubmed:affiliation
Department of Surgery, Ohio State University College of Medicine, Columbus 43210.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't