biostudies-literatureCooper DLNIHR Newcastle Biomedical Research CentreVersus ArthritisMedical Research CouncilNational Institute for Health Research (NIHR)e28918https://www.ebi.ac.uk/biostudies/studies/S-EPMC3250404biostudies-literatureUnknown7(1)<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 RAPloS oneFcγRIIIa expression on monocytes in rheumatoid arthritis: role in immune-complex stimulated TNF production and non-response to methotrexate therapy.PMC325040419764IS-BRC-0211-10046BH120307CL-2009-02-00218475NF-SI-0508-10299G1001518Fairclough ANunns CGill AHordon LHammond AEmery PAdebajo AMadden JHensor EBrown CTaylor LFirth JMcGonag DMartin MNeville BMartin SGRashid LHMelsom RDoherty SRobinson JIRhys-Evans BPease CHarvey ABejarano VMackie SLHelliwell PThomas CGough AKeenan AMCharles CJYEAR ConsortiumCooper DLJarrett SHenshaw KReece RIsaacs JDPadwell BNam JHuson GKitcheman JPickles DHeard JQuinn MKing HKarim ZGreen JConaghan PGreen MIsdale ASmith SMorgan AWCorscadden DSigsworth LCox SfalseFcγRIIIa expression on monocytes in rheumatoid arthritis: role in immune-complex stimulated TNF production and non-response to methotrexate therapy.<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 RA2012-01-01T00:00:00Z20122025-04-19T13:48:54.577Z2019-03-26T23:08:19ZS-EPMC32504042223525310.1371/journal.pone.0028918