Presence of an interferon signature in individuals who are anti-nuclear antibody positive lacking a systemic autoimmune rheumatic disease diagnosis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Joan Wither, Sindhu R. Johnson, Tony Liu, Babak Noamani, Dennisse Bonilla, Larissa Lisnevskaia, Earl Silverman, Arthur Bookman, Carolina Landolt-Marticorena

ABSTRACT

BACKGROUND: Elevated levels of type I interferons (IFNs) are a characteristic feature of the systemic autoimmune rheumatic diseases (SARDs) and are thought to play an important pathogenic role. However, it is unknown whether these elevations are seen in anti-nuclear antibody-positive (ANA+) individuals who lack sufficient criteria for a SARD diagnosis. We examined IFN-induced gene expression in asymptomatic ANA+ individuals and patients with undifferentiated connective tissue disease (UCTD) to address this question. METHODS: Healthy ANA- control subjects and ANA+ titre (≥1:160 by immunofluorescence) participants meeting no criteria, meeting at least one criterion (UCTD) or meeting SARD classification criteria were recruited. Whole peripheral blood IFN-induced and BAFF gene expression were quantified using NanoString technology. The normalized levels of five IFN-induced genes were summed to produce an IFN5 score. RESULTS: The mean IFN5 scores were increased in all ANA+ participant subsets as compared with healthy control subjects. We found that 36.8% of asymptomatic ANA+ and 50% of UCTD participants had IFN5 scores >2 SD above the mean for healthy control subjects. In all ANA+ subsets, the IFN5 score correlated with the presence of anti-Ro/La antibodies. In the asymptomatic ANA+ subset, this score also correlated with the ANA titre, whereas in the other ANA+ subsets, it correlated with the number of different ANA specificities. Development of new SARD criteria was seen in individuals with normal and high IFN5 scores. CONCLUSIONS: An IFN signature is seen in a significant proportion of ANA+ individuals and appears to be associated with ANA titre and type of autoantibodies, rather than with the presence or development of clinical SARD symptoms. More... »

PAGES

41

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s13075-017-1243-y

DOI

http://dx.doi.org/10.1186/s13075-017-1243-y

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1084252262

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28245862


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    "description": "BACKGROUND: Elevated levels of type I interferons (IFNs) are a characteristic feature of the systemic autoimmune rheumatic diseases (SARDs) and are thought to play an important pathogenic role. However, it is unknown whether these elevations are seen in anti-nuclear antibody-positive (ANA+) individuals who lack sufficient criteria for a SARD diagnosis. We examined IFN-induced gene expression in asymptomatic ANA+ individuals and patients with undifferentiated connective tissue disease (UCTD) to address this question.\nMETHODS: Healthy ANA- control subjects and ANA+ titre (\u22651:160 by immunofluorescence) participants meeting no criteria, meeting at least one criterion (UCTD) or meeting SARD classification criteria were recruited. Whole peripheral blood IFN-induced and BAFF gene expression were quantified using NanoString technology. The normalized levels of five IFN-induced genes were summed to produce an IFN5 score.\nRESULTS: The mean IFN5 scores were increased in all ANA+ participant subsets as compared with healthy control subjects. We found that 36.8% of asymptomatic ANA+ and 50% of UCTD participants had IFN5 scores >2 SD above the mean for healthy control subjects. In all ANA+ subsets, the IFN5 score correlated with the presence of anti-Ro/La antibodies. In the asymptomatic ANA+ subset, this score also correlated with the ANA titre, whereas in the other ANA+ subsets, it correlated with the number of different ANA specificities. Development of new SARD criteria was seen in individuals with normal and high IFN5 scores.\nCONCLUSIONS: An IFN signature is seen in a significant proportion of ANA+ individuals and appears to be associated with ANA titre and type of autoantibodies, rather than with the presence or development of clinical SARD symptoms.", 
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Download the RDF metadata as:  json-ld nt turtle xml License info

HOW TO GET THIS DATA PROGRAMMATICALLY:

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Turtle is a human-readable linked data format.

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RDF/XML is a standard XML format for linked data.

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1186/s13075-017-1243-y'


 

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308 https://www.grid.ac/institutes/grid.231844.8 schema:alternateName University Health Network
309 schema:name Krembil Research Institute, University Health Network, Toronto, ON, Canada
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311 https://www.grid.ac/institutes/grid.417188.3 schema:alternateName Toronto Western Hospital
312 schema:name Department of Immunology, University of Toronto, Toronto, ON, Canada
313 Department of Medicine, University of Toronto, Toronto, ON, Canada
314 Division of Rheumatology, University Health Network, Toronto, ON, Canada
315 Krembil Research Institute, University Health Network, Toronto, ON, Canada
316 Toronto Western Hospital, 1E-420, 399 Bathurst Street, M5T 2S8, Toronto, ON, Canada
317 rdf:type schema:Organization
 




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