Linked Life Data

18369625

Source:http://linkedlifedata.com/resource/pubmed/id/18369625

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2008-7-11
pubmed:abstractText
Ankylosing spondylitis (AS) is characterized by ankylosis of axial joints but osteoporosis is also a well-reported feature. T cells have been implicated as a source of receptor activator of NFkappaB ligand (RANKL) in inflammatory bone diseases. Hence, we assessed whether T cells in patients with AS act as a source of RANKL too. Therefore, we investigated the expression of RANKL on T cells from 21 patients with AS by flow cytometry. Bone mineral density (BMD) was evaluated by quantitative computer tomography (QCT) and dual X-ray absorptiometry (DXA) and correlated with serum levels of osteoprotegerin (OPG) and RANKL. BMD was decreased in 45% of all patients when measured with DXA (48% with QCT) and correlated negatively with OPG. Expression of intracellular RANKL was increased on CD4+ (84 vs. 70%) and CD8+ (85.2 vs. 65.3%, P < 0.05) T cells in patients with AS, whereas expression of membrane-bound RANKL was significantly lower (CD4+: 2.2 vs. 8.5% and CD8+: 0.7 vs. 3.2%, P < 0.01). Our results indicate that surface and intracellular RANKL production is differentially regulated on T cells of patients with AS.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0172-8172
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
987-93
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Intracellular and surface RANKL are differentially regulated in patients with ankylosing spondylitis.
pubmed:affiliation
Department of Pathophysiology, Center of Physiology and Pathophysiology, Medical University of Vienna, Vienna, Austria. daniela.stupphann@meduniwien.ac.at
pubmed:publicationType
Journal Article