Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-10-28
pubmed:abstractText
We recently demonstrated that functional NK cells are produced from their precursors in murine long-term bone marrow cultures without the addition of exogenous growth factors. Because IL-7 is known to be produced by bone marrow stromal cells and is a proliferation factor for some immature cells of the B and T cell lineages, we tested whether rIL-7 could support the proliferation or maturation of NK precursor cells. By itself, rIL-7 did not induce NK lytic activity in cultures of unseparated bone marrow cells (BMC), but it did augment the response of unseparated BMC to 50 U rIL-2/ml, with a maximal enhancement at 10 ng IL-7/ml. Depletion experiments demonstrated that the IL-7-induced increase in cytotoxicity was not due to NK precursors, however, but to mature T and NK cells. IL-7 preferentially increased the number of CD8+ cells. Preculture of NK 1.1-depleted BMC with IL-7 did not increase the total number of NK 1.1+ cells or the lytic activity generated from NK precursor cells. However, IL-2-responsive NK lineage cells survived better in IL-7-supplemented medium than in medium alone. Thus, soluble rIL-7 did not expand the NK precursor cell population in vitro but it maintained the viability and subsequent responsiveness to IL-2 of NK precursors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0008-8749
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
151
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-11
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Effects of rIL-7 on murine bone marrow NK precursor cells.
pubmed:affiliation
Department of Biological Structure, School of Medicine, University of Washington, Seattle 98195.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.