{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cooper DL"],"funding":["NIHR Newcastle Biomedical Research Centre","Versus Arthritis","Medical Research Council","National Institute for Health Research (NIHR)"],"pagination":["e28918"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3250404"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(1)"],"pubmed_abstract":["<h4>Objective</h4>The expression of FcγRIIIa/CD16 may render monocytes targets for activation by IgG-containing immune complexes (IC). We investigated whether FcγRIIIa/CD16 was upregulated in rheumatoid arthritis (RA), associated with TNF production in response to IC-stimulation, and if this predicted response to methotrexate therapy.<h4>Methods</h4>FcγRIIIa/CD16 expression on CD14(low) and CD14++ monocytes was measured by flow cytometry in healthy controls and RA patients (early and long-standing disease). Intracellular TNF-staining was carried out after in vitro LPS or heat-aggregated immunoglobulin (HAG) activation. FcγRIIIa/CD16 expression pre- and post-steroid/methotrexate treatment was examined.<h4>Results</h4>Increased FcγRIIIa/CD16 expression on CD14++ monocytes in long-standing RA"],"journal":["PloS one"],"pubmed_title":["FcγRIIIa expression on monocytes in rheumatoid arthritis: role in immune-complex stimulated TNF production and non-response to methotrexate therapy."],"pmcid":["PMC3250404"],"funding_grant_id":["19764","IS-BRC-0211-10046","BH120307","CL-2009-02-002","18475","NF-SI-0508-10299","G1001518"],"pubmed_authors":["Fairclough A","Nunns C","Gill A","Hordon L","Hammond A","Emery P","Adebajo A","Madden J","Hensor E","Brown C","Taylor L","Firth J","McGonag D","Martin M","Neville B","Martin SG","Rashid LH","Melsom R","Doherty S","Robinson JI","Rhys-Evans B","Pease C","Harvey A","Bejarano V","Mackie SL","Helliwell P","Thomas C","Gough A","Keenan AM","Charles CJ","YEAR Consortium","Cooper DL","Jarrett S","Henshaw K","Reece R","Isaacs JD","Padwell B","Nam J","Huson G","Kitcheman J","Pickles D","Heard J","Quinn M","King H","Karim Z","Green J","Conaghan P","Green M","Isdale A","Smith S","Morgan AW","Corscadden D","Sigsworth L","Cox S"],"additional_accession":[]},"is_claimable":false,"name":"FcγRIIIa expression on monocytes in rheumatoid arthritis: role in immune-complex stimulated TNF production and non-response to methotrexate therapy.","description":"<h4>Objective</h4>The expression of FcγRIIIa/CD16 may render monocytes targets for activation by IgG-containing immune complexes (IC). We investigated whether FcγRIIIa/CD16 was upregulated in rheumatoid arthritis (RA), associated with TNF production in response to IC-stimulation, and if this predicted response to methotrexate therapy.<h4>Methods</h4>FcγRIIIa/CD16 expression on CD14(low) and CD14++ monocytes was measured by flow cytometry in healthy controls and RA patients (early and long-standing disease). Intracellular TNF-staining was carried out after in vitro LPS or heat-aggregated immunoglobulin (HAG) activation. FcγRIIIa/CD16 expression pre- and post-steroid/methotrexate treatment was examined.<h4>Results</h4>Increased FcγRIIIa/CD16 expression on CD14++ monocytes in long-standing RA","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012","modification":"2025-04-19T13:48:54.577Z","creation":"2019-03-26T23:08:19Z"},"accession":"S-EPMC3250404","cross_references":{"pubmed":["22235253"],"doi":["10.1371/journal.pone.0028918"]}}