Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-1-15
pubmed:abstractText
Soluble forms of HLA-G (sHLA-G) have been implicated in immune regulation. Fetal trophoblast cells are a prime source of HLA-G. Hence, an interaction between sHLA-G and uterine lymphocytes in the decidual tissues can easily be envisaged. These lymphocytes, when properly activated, are implicated in successful trophoblast invasion, placental maturation and maintenance of pregnancy. However, so far, no data are available on the effect of sHLA-G on the function and phenotype of these cells. Herein, we used a recombinant sHLA-G construct to determine the effect of sHLA-G on uterine lymphocyte cells present in endometrium at the time that it is optimally receptive to trophoblast invasion. In addition, we ascertained the effect of sHLA-G on peripheral lymphocytes. We found that upon co-culture with sHLA-G, proliferation of unfractionated IL-15-stimulated uterine mononuclear cells (UMCs) was inhibited. However, sHLA-G increased both interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha production by these cells. Vascular endothelial growth factor (VEGF) production was reduced. Notably, in contrast to membrane-bound HLA-G, sHLA-G did not affect the natural cytolytic activity of UMCs. Similarly, sHLA-G inhibited proliferation but stimulated pro-inflammatory cytokine production by cytokine-activated, unfractionated peripheral blood mononuclear cells (PBMCs). In addition, we showed that the overall inhibitory effect of sHLA-G on proliferation of the whole cell population could be ascribed to selective inhibition of CD4(+) T cells. In contrast, sHLA-G induced proliferation and IFN-gamma production by both uterine and peripheral natural killer (NK) cells. In conclusion, our data show that the sHLA-G modulates both UMC and PBMC function. sHLA-G, by promoting IFN-gamma production by uterine NK cells, may contribute to vascular remodelling of spiral arteries to allow for successful embryo implantation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1360-9947
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
123-33
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:17121749-Animals, pubmed-meshheading:17121749-CHO Cells, pubmed-meshheading:17121749-Cell Proliferation, pubmed-meshheading:17121749-Cells, Cultured, pubmed-meshheading:17121749-Cricetinae, pubmed-meshheading:17121749-Cricetulus, pubmed-meshheading:17121749-Female, pubmed-meshheading:17121749-HLA Antigens, pubmed-meshheading:17121749-HLA-G Antigens, pubmed-meshheading:17121749-Histocompatibility Antigens Class I, pubmed-meshheading:17121749-Humans, pubmed-meshheading:17121749-Immunity, Cellular, pubmed-meshheading:17121749-Interferon-gamma, pubmed-meshheading:17121749-K562 Cells, pubmed-meshheading:17121749-Killer Cells, Natural, pubmed-meshheading:17121749-Solubility, pubmed-meshheading:17121749-Th1 Cells, pubmed-meshheading:17121749-Tumor Necrosis Factor-alpha, pubmed-meshheading:17121749-Uterus
pubmed:year
2007
pubmed:articleTitle
Soluble HLA-G promotes Th1-type cytokine production by cytokine-activated uterine and peripheral natural killer cells.
pubmed:affiliation
Department of Bloodtransfusion and Transplantation Immunology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. a.vandermeer@abti.umcn.nl
pubmed:publicationType
Journal Article