Investigation of type I interferon responses in ANCA-associated vasculitis

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 inflammation in these conditions. Anti-neutrophil cytoplasmic antibody (ANCA)-Assoc...

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Autores principales:	Isabella Batten, Mark W. Robinson, Arthur White, Cathal Walsh, Barbara Fazekas, Jason Wyse, Antonia Buettner, Suzanne D’Arcy, Emily Greenan, Conor C. Murphy, Zoe Wigston, Joan Ní Gabhann-Dromgoole, Edward M. Vital, Mark A. Little, Nollaig M. Bourke
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/0b1c1eccbc1e48ba9d209eb9887c08a1
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spelling	oai:doaj.org-article:0b1c1eccbc1e48ba9d209eb9887c08a12021-12-02T14:26:25ZInvestigation of type I interferon responses in ANCA-associated vasculitis10.1038/s41598-021-87760-42045-2322https://doaj.org/article/0b1c1eccbc1e48ba9d209eb9887c08a12021-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-87760-4https://doaj.org/toc/2045-2322Abstract 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 inflammation in these conditions. Anti-neutrophil cytoplasmic antibody (ANCA)-Associated Vasculitis (AAV) is an autoimmune disease characterised by necrotising inflammation 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.Isabella BattenMark W. RobinsonArthur WhiteCathal WalshBarbara FazekasJason WyseAntonia BuettnerSuzanne D’ArcyEmily GreenanConor C. MurphyZoe WigstonJoan Ní Gabhann-DromgooleEdward M. VitalMark A. LittleNollaig M. BourkeNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Isabella Batten Mark W. Robinson Arthur White Cathal Walsh Barbara Fazekas Jason Wyse Antonia Buettner Suzanne D’Arcy Emily Greenan Conor C. Murphy Zoe Wigston Joan Ní Gabhann-Dromgoole Edward M. Vital Mark A. Little Nollaig M. Bourke Investigation of type I interferon responses in ANCA-associated vasculitis
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 inflammation in these conditions. Anti-neutrophil cytoplasmic antibody (ANCA)-Associated Vasculitis (AAV) is an autoimmune disease characterised by necrotising inflammation 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.
format	article
author	Isabella Batten Mark W. Robinson Arthur White Cathal Walsh Barbara Fazekas Jason Wyse Antonia Buettner Suzanne D’Arcy Emily Greenan Conor C. Murphy Zoe Wigston Joan Ní Gabhann-Dromgoole Edward M. Vital Mark A. Little Nollaig M. Bourke
author_facet	Isabella Batten Mark W. Robinson Arthur White Cathal Walsh Barbara Fazekas Jason Wyse Antonia Buettner Suzanne D’Arcy Emily Greenan Conor C. Murphy Zoe Wigston Joan Ní Gabhann-Dromgoole Edward M. Vital Mark A. Little Nollaig M. Bourke
author_sort	Isabella Batten
title	Investigation of type I interferon responses in ANCA-associated vasculitis
title_short	Investigation of type I interferon responses in ANCA-associated vasculitis
title_full	Investigation of type I interferon responses in ANCA-associated vasculitis
title_fullStr	Investigation of type I interferon responses in ANCA-associated vasculitis
title_full_unstemmed	Investigation of type I interferon responses in ANCA-associated vasculitis
title_sort	investigation of type i interferon responses in anca-associated vasculitis
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/0b1c1eccbc1e48ba9d209eb9887c08a1
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Investigation of type I interferon responses in ANCA-associated vasculitis

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