Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1988-11-14
pubmed:abstractText
It is likely that immune cells in the bone marrow produce factors which are involved in the local control of bone remodeling. Immune cell products such as interleukin-1 and the tumor necrosis factors are potent stimulators of bone resorption in vitro. In this paper, we have studied the effects of recombinant murine interferon-gamma on bone resorption stimulated by these agents and the systemic calcium-regulating hormones 1,25(OH)2 vitamin D3 and parathyroid hormone. We found that interferon-gamma completely abolished bone resorption stimulated by the cytokines interleukin-1, tumor necrosis factor alpha and tumor necrosis factor beta. In contrast, parathyroid hormone- and 1,25(OH)2 vitamin D3-stimulated bone resorption were not significantly affected by the addition of interferon-gamma under the same conditions. Parathyroid hormone-stimulated bone resorption was inhibited slightly when larger concentrations of interferon-gamma were used for more prolonged periods. The inhibitory effects on cytokine-stimulated bone resorption occurred at interferon concentrations of 100 U/ml (half-maximal) to 300 U/ml (complete inhibition). This relatively selective inhibition of cytokine-stimulated bone resorption by an immune cell product may have physiological significance in the local control of trabecular bone volume and bone remodeling.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0884-0431
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
469-74
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
Preferential inhibition of cytokine-stimulated bone resorption by recombinant interferon gamma.
pubmed:affiliation
Department of Medicine, University of Texas Health Science Center, San Antonio 72884.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.