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Comparison of Surro...
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Enocsson, HelenaLinköpings universitet,Linköping University,Linköping Univ, Dept Biomed & Clin Sci, Div Inflammat & Infect, Linköping, Sweden.,Avdelningen för inflammation och infektion,Medicinska fakulteten
(författare)
Comparison of Surrogate Markers of the Type I Interferon Response and Their Ability to Mirror Disease Activity in Systemic Lupus Erythematosus
- Artikel/kapitelEngelska2021
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2021-06-30
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Frontiers Media S.A.2021
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electronicrdacarrier
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LIBRIS-ID:oai:DiVA.org:uu-452362
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-452362URI
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https://doi.org/10.3389/fimmu.2021.688753DOI
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https://lup.lub.lu.se/record/1f3f8d1e-37de-48e4-9a89-71dea3e317b7URI
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https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-180063URI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:art swepub-publicationtype
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Funding Agencies|Swedish Rheumatism association [R-844801]; Region Ostergotland ALF Grants [LIO-791961]; King Gustaf Vs 80-year Anniversary Foundation [FAI-2018-0504]; King Gustaf V, Queen Victorias Foundation of Freemasons; Alfred Osterlunds Foundation; Anna-Greta Crafoord Foundation; Greta and Johan Kocks Foundation; Skane University Hospital; Medical Faculty of Lund University; Swedish Research Council for Medicine and Health [2018-02399, 2018-02516, 2017-01091]
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Objectives: Type I interferons (IFNs) are central and reflective of disease activity in systemic lupus erythematosus (SLE). However, IFN-alpha levels are notoriously difficult to measure and the type I IFN gene signature (IGS) is not yet available in clinical routine. This study evaluates galectin-9 and an array of chemokines/cytokines in their potential as surrogate markers of type I IFN and/or SLE disease activity.Methods: Healthy controls and well-characterized Swedish SLE patients from two cross-sectional cohorts (n=181; n=59) were included, and a subgroup (n=21) was longitudinally followed. Chemokine/cytokine responses in immune complex triggered IFN-alpha activity was studied in healthy donor peripheral blood mononuclear cells (PBMC). Levels of chemokines/cytokines and galectin-9 were measured by immunoassays. Gene expression was quantified by qPCR.Results: The IGS was significantly (p<0.01) correlated with galectin-9 (rho=0.54) and CXCL10 (rho=0.37) levels whereas serum IFN-alpha correlated with galectin-9 (rho=0.36), CXCL10 (rho=0.39), CCL19 (rho=0.26) and CCL2 (rho=0.19). The strongest correlation was observed between galectin-9 and TNF (rho=0.56). IFN-alpha and disease activity (SLEDAI-2K) were correlated (rho=0.20) at cross-sectional analysis, but no significant associations were found between SLEDAI-2K and galectin-9 or chemokines. Several inflammatory mediators increased at disease exacerbation although CCL19, CXCL11, CXCL10, IL-10 and IL-1 receptor antagonist were most pronounced. Immune complex-stimulation of PBMC increased the production of CCL2, CXCL8 and TNF.Conclusion: Galectin-9 and CXCL10 were associated with type I IFN in SLE but correlated stronger with TNF. None of the investigated biomarkers showed a convincing association with disease activity, although CXCL10 and CCL19 performed best in this regard.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Wetterö, JonasLinköpings universitet,Linköping University,Linköping Univ, Dept Biomed & Clin Sci, Div Inflammat & Infect, Linköping, Sweden.,Avdelningen för inflammation och infektion,Medicinska fakulteten(Swepub:liu)jonwe26
(författare)
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Eloranta, Maija-LeenaUppsala University,Uppsala universitet,Reumatologi,Uppsala Univ, Sweden(Swepub:uu)maelo020
(författare)
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Gullstrand, BirgittaLund University,Lunds universitet,Reumatologi och molekylär skelettbiologi,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Lund SLE Research Group,Forskargrupper vid Lunds universitet,Barnreumatologiskt forskningscentrum,Rheumatology,Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Lund University Research Groups,Center of Pediatric Rheumatology,Lund Univ, Dept Clin Sci Lund, Div Rheumatol, Lund, Sweden.(Swepub:lu)mmb-bgu
(författare)
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Svanberg, CeciliaLinköpings universitet,Linköping University,Linköping Univ, Dept Biomed & Clin Sci, Div Mol Med & Virol, Linköping, Sweden.,Avdelningen för molekylär medicin och virologi,Medicinska fakulteten(Swepub:liu)cecsv36
(författare)
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Larsson, MarieLinköpings universitet,Linköping University,Linköping Univ, Dept Biomed & Clin Sci, Div Mol Med & Virol, Linköping, Sweden.,Avdelningen för molekylär medicin och virologi,Medicinska fakulteten(Swepub:liu)marla67
(författare)
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Bengtsson, Anders A.Lund University,Lunds universitet,Reumatologi och molekylär skelettbiologi,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Rheumatology,Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Lund Univ, Dept Clin Sci Lund, Div Rheumatol, Lund, Sweden.(Swepub:lu)reum-abe
(författare)
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Rönnblom, LarsUppsala University,Uppsala universitet,Reumatologi,Uppsala Univ, Sweden(Swepub:uu)larsronn
(författare)
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Sjöwall, ChristopherLinköpings universitet,Linköping University,Linköping Univ, Dept Biomed & Clin Sci, Div Inflammat & Infect, Linköping, Sweden.,Avdelningen för inflammation och infektion,Medicinska fakulteten,Region Östergötland, Reumatologiska kliniken i Östergötland(Swepub:liu)chrsj93
(författare)
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Linköping UniversityLinköping Univ, Dept Biomed & Clin Sci, Div Inflammat & Infect, Linköping, Sweden.
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Ingår i:Frontiers in Immunology: Frontiers Media S.A.121664-3224
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