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Investigation of type I interferon responses in ANCA‑associated vasculitis

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dc.contributor.author Batten, Isabella
dc.contributor.author Robinson, Mark W.
dc.contributor.author White, Arthur
dc.contributor.author Walsh, Cathal Dominic
dc.contributor.author Fazekas, Barbara
dc.contributor.author Wyse, Jason
dc.contributor.author Buettner, Antonia
dc.contributor.author D’Arcy, Suzanne
dc.contributor.author Greenan, Emily
dc.contributor.author Murphy, Conor C.
dc.contributor.author Wigston, Zoe
dc.contributor.author Ní Gabhann‑Dromgoole, Joan
dc.contributor.author Vital, Edward M.
dc.contributor.author Little, Mark A.
dc.contributor.author Bourke, Nollaig M.
dc.date.accessioned 2021-04-23T08:44:21Z
dc.date.available 2021-04-23T08:44:21Z
dc.date.issued 2021
dc.identifier.uri http://hdl.handle.net/10344/10026
dc.description peer-reviewed en_US
dc.description.abstract Type I interferon (IFN) dysregulation is a major contributory factor in the development of several autoimmune diseases, termed type I interferonopathies, and is thought to be the pathogenic link with chronic infammation in these conditions. Anti-neutrophil cytoplasmic antibody (ANCA)-Associated Vasculitis (AAV) is an autoimmune disease characterised by necrotising infammation of small blood vessels. The underlying biology of AAV is not well understood, however several studies have noted abnormalities in type I IFN responses. We hypothesised that type I IFN responses are systemically dysregulated in AAV, consistent with features of a type I interferonopathy. To investigate this, we measured the expression of seven interferon regulated genes (IRGs) (ISG15, SIGLEC1, STAT1, RSAD2, IFI27, IFI44L and IFIT1) in peripheral blood samples, as well as three type I IFN regulated proteins (CXCL10, MCP-1 and CCL19) in serum samples from AAV patients, healthy controls and disease controls. We found no difference in type I IFN regulated gene or protein expression between AAV patients and healthy controls. Furthermore, IRG and IFN regulated protein expression did not correlate with clinical measurements of disease activity in AAV patients. Thus, we conclude that systemic type I IFN responses are not key drivers of AAV pathogenesis and AAV should not be considered a type I interferonopathy. en_US
dc.language.iso eng en_US
dc.publisher Nature en_US
dc.relation 208591 en_US
dc.relation.ispartofseries Scientifc Reports;11, 8272
dc.subject AAV pathogenesis en_US
dc.subject autoimmune en_US
dc.title Investigation of type I interferon responses in ANCA‑associated vasculitis en_US
dc.type info:eu-repo/semantics/article en_US
dc.type.supercollection all_ul_research en_US
dc.type.supercollection ul_published_reviewed en_US
dc.identifier.doi 10.1038/s41598-021-87760-4
dc.contributor.sponsor SFI en_US
dc.contributor.sponsor Meath Foundation en_US
dc.relation.projectid 11/Y/B2093 en_US
dc.relation.projectid 208591 en_US
dc.rights.accessrights info:eu-repo/semantics/openAccess en_US


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