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dc.contributor.authorWade, Sarah M
dc.contributor.authorCanavan, Mary
dc.contributor.authorMcGarry, Trudy
dc.contributor.authorLow, Candice
dc.contributor.authorWade, Siobhan C
dc.contributor.authorMullan, Ronan H
dc.contributor.authorVeale, Douglas J
dc.contributor.authorFearon, Ursula
dc.date.accessioned2020-02-24T14:52:40Z
dc.date.available2020-02-24T14:52:40Z
dc.date.issued2019-01-09
dc.identifier.pmid30626658
dc.identifier.doi10.1136/annrheumdis-2018-214138
dc.identifier.urihttp://hdl.handle.net/10147/627220
dc.description.abstractPsA synovial tissue infiltrating CD4+ T-cells expressed higher levels of interleukin (IL)-17A, interferon gamma (IFN-γ), GM-CSF and CD161, with parallel enrichment of Th1, Th17 and exTh17 T-helper subsets (all p<0.05). Interestingly, a significant proportion of synovial T-cell subsets were triple-positive for GM-CSF, tumour necrosis factor (-TNF), -IL-17 or IFN-γ compared with matched blood (all p<0.05). Importantly, frequencies of polyfunctional T-cells correlated with DAPSA: Th1-GM-CSF+/TNF+/IFN-γ+ (r=0.7, p<0.01), Th17-GM-CSF+/TNF+/IL-17+ (r=0.6, p<0.057) and exTh17-GM-CSF+/TNF+/IFN-γ+ (r=0.7, p=0.0096), with no associations observed for single cytokine-producing T-cells. Following ex vivo culture of PsA synovial tissue cell suspensions, polyfunctional GM-CSF+TNFα+IL-17A+ or/IFN-γ+-producing T-cells (p<0.05), but not single cytokine-producing T-cells, were inhibited with a PDE4 inhibitor. Conclusion: These data demonstrate enrichment of polyfunctional T-cells in PsA synovial tissue which were strongly associated with DAPSA and ex vivo therapeutic response.en_US
dc.language.isoenen_US
dc.rights© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
dc.subjectpolyfunctional t-cellsen_US
dc.subjectpsoriatic arthritisen_US
dc.subjectsynovial tissueen_US
dc.subjectCELL BIOLOGYen_US
dc.titleAssociation of synovial tissue polyfunctional T-cells with DAPSA in psoriatic arthritis.en_US
dc.typeArticleen_US
dc.typeOtheren_US
dc.identifier.eissn1468-2060
dc.identifier.journalAnnals of the rheumatic diseasesen_US
dc.description.peer-reviewpeer-reviewen_US
dc.source.journaltitleAnnals of the rheumatic diseases
dc.source.volume78
dc.source.issue3
dc.source.beginpage350
dc.source.endpage354
refterms.dateFOA2020-02-24T14:52:41Z
dc.source.countryEngland


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