Cited by 220Systemic Lupus Erythematosus ResearchSystemic Sclerosis and Related Diseasesinterferon and immune responses

The interferon-α signature of systemic lupus erythematosus

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Obermoser, G., Pascual, V.·2010·Lupus

Abstract

Systemic lupus erythematosus (SLE) is a prototypic multisystem autoimmune disorder where interplay of environmental and genetic risk factors leads to progressive loss of tolerance to nuclear antigens over time, finally culminating in clinical disease. The heterogeneity of clinical manifestations and the disease’s unpredictable course characterized by flares and remissions are very likely a reflection of heterogeneity at the origin of disease, with a final common pathway leading to loss of tolerance to nuclear antigens. Impaired clearance of immune complexes and apoptotic material and production of autoantibodies have long been recognized as major pathogenic events in this disease. Over the past decade the type I interferon cytokine family has been postulated to play a central role in SLE pathogenesis, by promoting feedback loops progressively disrupting peripheral immune tolerance and driving disease activity. The identification of key molecules involved in the pathogenesis of SLE will not only improve our understanding of this complex disease, but also help to identify novel targets for biological intervention. Lupus (2010) 19, 1012—1019.

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  • Many of the changes in the circulating proteome in people with Down syndrome are highly reminiscent of those observed in type I interferonopathies and other autoinflammatory conditions.

    “Our study of the circulating proteome in people with DS, the largest and most comprehensive study of this kind reported to date, reveals that T21 causes profound immune dysregulation, with many of the changes being highly reminiscent of those observed in type I interferonopathies and other autoinflammatory conditions54,58–60,88 (Table 1).”

    From Trisomy 21 causes changes in the circulating proteome indicative of chronic autoinflammation (2017) · cites this paper as [54]

    The section “The IFN-α signature of SLE” reports elevated interferon and upregulated interferon-regulated transcripts in the blood of people with lupus, supporting an analogy to interferon-associated immune changes. It does not examine the circulating proteome in Down syndrome or establish that its protein changes resemble those in lupus or other conditions. (LLM, conf=0.82)

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Authors
Obermoser, G., & Pascual, V.
Affiliations
  • Innsbruck Medical University (AT)
  • Baylor Institute for Immunology Research, Dallas, TX, USA,
Venue
Lupus
Published
2010-08
Volume
19
Issue
9
Pages
1012-1019
ISSN
  • 0961-2033 (ISSN-L)
  • 1477-0962
OpenAlex
W2117832897
Cited by
220
References
3
Citations by year
2026: 7 · 2025: 6 · 2024: 7 · 2023: 6 · 2022: 7 · 2021: 12 · 2020: 12 · 2019: 17 · 2018: 14 · 2017: 17 · 2016: 20 · 2015: 19 · 2014: 19 · 2013: 23 · 2012: 19
FWCI
2.41
Type
journal article
Language
en
Open access
Locations
  • Lupus (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute of Allergy and Infectious Diseases (U19AI082715, U19-AI082715-01)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR050770, P50AR055503, P50AR054083, AR055503-01CORT, AR054083-01CORT)
Topics
  • Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Systemic Sclerosis and Related Diseases
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
Keywords
systemic lupus erythematosus, type I interferon, interferon signature, autoimmunity, immune tolerance, nuclear antigens, immune complexes, efferocytosis, autoantibodies, disease heterogeneity, SLE pathogenesis, therapeutic target
MeSH terms
Animals, Autoantibodies, Humans, Immune Tolerance, Interferon Type I, Lupus Erythematosus, Systemic, Interferon-alpha, Apoptosis, Antigens, Nuclear

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