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- aggregation classification "A1".
- aggregation creator B675020.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation date "2014".
- aggregation format "application/pdf".
- aggregation hasFormat 4094286.bibtex.
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- aggregation hasFormat 4094286.yaml.
- aggregation isPartOf urn:issn:0003-4967.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Medicine and Health Sciences".
- aggregation title "Senescence marker killer cell lectin-like receptor G1 (KLRG1) contributes to TNF-α production by interaction with its soluble E-cadherin ligand in chronically inflamed joints".
- aggregation abstract "Objectives: Killer cell lectin-like receptor G1 (KLRG1) is an NK cell marker also expressed on T cells showing an immunosenescent phenotype. KLRG1 binding to its ligand E-cadherin inhibits functional responses. It was recently shown that soluble E-cadherin (sE-cadherin) also influences KLRG1 signalling, although its involvement in arthritis is unknown. Our goal was to evaluate the contribution of KLRG1(+) T cells to synovitis. Methods: Paired peripheral blood (PB) and synovial fluid (SF) mononuclear cells from 21 patients with spondyloarthritis (SpA) or rheumatoid arthritis (RA), eight with crystal-induced arthritis and 10 controls were obtained. T cells were characterised for KLRG1 expression directly ex vivo, while TNF-alpha/IFN-gamma production was assessed after polyclonal stimulation. Assays of chemotaxis response towards SF were conducted. Additionally, sE-cadherin levels in our paired samples were determined. Moreover, TNF-alpha/IFN-gamma production by antigen-specific T cells was evaluated in the presence of sE-cadherin. Results: KLRG1(+) T cells were enriched in SF as opposed to PB of SpA and RA patients, which contrasts with results obtained in crystal-induced arthritides. KLRG1(+) T cells were more functionally active as opposed to KLRG1-T cells and migrated preferentially towards SpA and RA SF. sE-cadherin levels were higher in SF versus plasma. The presence of sE-cadherin enhanced the number of KLRG1(+) CD4(+) T cells able to produce TNF-alpha but not IFN-gamma. Conclusions: sE-cadherin contributes to the local proinflammatory environment in the joint by favouring TNF-a production by KLRG1(+) CD4(+) T cells. This pathway seems to be operational in both SpA and RA, but not in crystal-induced arthritis.".
- aggregation authorList BK1036900.
- aggregation endPage "1231".
- aggregation issue "6".
- aggregation startPage "1223".
- aggregation volume "73".
- aggregation aggregates 5919935.
- aggregation isDescribedBy 4094286.
- aggregation similarTo annrheumdis-2013-203881.
- aggregation similarTo LU-4094286.