Linked Life Data

9430508

Source:http://linkedlifedata.com/resource/pubmed/id/9430508

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-2-4
pubmed:abstractText
The goal of the present work was to study the regulatory role of T lymphocytes on natural killer (NK) cell generation in NK long-term bone marrow cultures (LTBMCs), an established mouse long-term bone marrow (BM) culture system used for the study of NK cell differentiation from precursors. Activation of the few T cells present in NK-LTBMCs by addition of anti-CD3 monoclonal antibody (mAb) together with interleukin (IL)-2 inhibited the generation of NK cells. Coculture with NK-LTBMCs of a pure population of preactivated BM T cells completely inhibited NK cell development even when the T cells were separated from the NK-LTBMCs by transwells. Depletion of IL-2 by activated T cells was not the mechanism of the negative regulation because anti-CD3 mAb added to the cultures inhibited the generation of NK cells even in the presence of 10-fold higher concentrations of exogenous IL-2 than that used in controls. Medium from cultures in which suppression had occurred was also suppressive, suggesting that one or more soluble factors released in the medium was responsible. That this effect was exerted on NK cell development from precursors was indicated by the finding that T cell-conditioned medium stimulated proliferation of mature NK cells. In our experimental conditions, monoclonal antibodies to IL-10, IL-13, transforming growth factor-beta, and tumor necrosis factor receptor failed to reverse the inhibitory effect.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0301-472X
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Suppression of natural killer cell differentiation by activated T lymphocytes in long-term cultures of mouse bone marrow.
pubmed:affiliation
Department of Clinical Medicine, Pathology, and Pharmacology, University of Perugia, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't