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oai:cora.ucc.ie:10468/99392023-03-31T07:18:26Zcom_10468_386com_10468_4com_10468_848com_10468_1col_10468_387col_10468_1186col_10468_8983

openaccess Molloy, Michael G. Stack, John icare 2020-05-13T09:12:40Z 2020-05-13T09:12:40Z 2020-02-18 2020-02-18 This body of work draws on parallels between the pathogenesis of rheumatoid arthritis (RA) and atherosclerosis. The pathogenesis and genetic basis of both diseases are described and compared. I describe how a polymorphism of the CX3CR1 gene, which has been shown to have a protective association against atherosclerosis, is shown to have has a similar protective association against RA. Using immunohistochemistry and confocal microscopy, I demonstrate that monocytes co-localise with CX3CR1 in human RA synovium, providing further evidence of the chemotactic effects between monocytes and the FKN/CX3CR1 axis and the significance of CX3CR1 in RA pathogenesis. Finally, I describe an association between seropositive RA and soluble Glycoprotein VI (sGPVI), a specific marker of platelet activation, providing further evidence that platelet activation is associated with seropositive RA and is likely antibody mediated. Together this body of work identifies shared pathogenic mechanisms between RA and atherosclerosis and identifies potential therapeutic targets for both RA and atherosclerosis. Not peer reviewed Accepted Version application/pdf Stack, J. R. 2020. Rheumatoid arthritis and atherosclerosis: common pathogenic mechanisms explored. MD Thesis, University College Cork. 81 https://hdl.handle.net/10468/9939 en University College Cork © 2020, John R. Stack. https://creativecommons.org/licenses/by-nc-nd/4.0/ Rheumatoid arthritis CX3CR1 GPVI Atherosclerosis Soluble GPVI Genetic case control study Biomarker Rheumatoid arthritis and atherosclerosis: common pathogenic mechanisms explored Doctoral thesis Doctoral MD - Doctor of Medicineinfo:eu-repo/semantics/openAccess