Evidence map›Paper›PMID 19968664›Full record

ArticleClinical and experimental immunology2010

Interferon signature gene expression is correlated with autoantibody profiles in patients with incomplete lupus syndromes.

Q-Z Li, J Zhou, Y Lian, B Zhang, V K Branch, F Carr-Johnson, D R Karp, C Mohan, E K Wakeland, N J Olsen

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

72 citing papers in PubMed, 2 syntheses or guidelines pooled it, 153 citations in OpenAlex.

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  17. Cell type-specific mechanistic target of rapamycin-dependent distortion of autophagy pathways in lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022
    Review
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12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Q-Z LiDepartment of Immunology and Division of Rheumatic Diseases, University of Texas Southwestern Medical Center, Dallas, TX 75390-8884, USA. quan.li@utsouthwestern.edu
J Zhou
Y Lian
B Zhang
V K Branch
F Carr-Johnson
D R Karp
C Mohan
E K Wakeland
N J Olsen
The University of Texas Southwestern Medical Center · US

Funding

SLAM Genes-from Mouse to ManP50AR055503 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI KARP, DAVID R · 2007 to 2011
$8.3M
NIAMS NIH HHS NIAMS/NIH P50AR055503NIAMS NIH HHS P50 AR055503
6 · The paper itself

Abstract

Interferon (IFN) signature genes have been shown to be expressed highly in peripheral blood of patients with systemic lupus erythematosus (SLE), especially in the presence of active disease. However, the expression of this gene signature in individuals with incomplete forms of lupus and the pathogenic relationship between IFN signature genes and autoantibody production have not been explored fully. In the present study, we examined the gene expression and autoantibody profiles of patients diagnosed with incomplete lupus erythematosus (ILE) to determine correlations of the gene expression signature with autoantibody production. Gene expression analysis was carried out on the 24K Illumina Human Refseq-8 arrays using blood samples from 84 subjects, including patients with SLE (n = 27) or ILE (n = 24), first-degree relatives (FDR) of these patients (n = 22) and non-autoimmune control (NC) individuals (n = 11). Autoantibody expression was measured using standard immunoassays and autoantigen proteomic arrays. Up-regulation of a set of 63 IFN signature genes was seen in 83% of SLE patients and 50% of ILE patients. High levels of IFN gene expression in ILE and SLE showed significant correlations with the expression of a subset of IgG autoantibodies, including chromatin, dsDNA, dsRNA, U1snRNP, Ro/SSA, La/SSB, topoisomerase I and Scl 70, while low IFN levels were correlated with immunoglobulin (Ig)M autoreactivity. These studies suggest that in patients with ILE the IFN gene expression signature may identify a subset of these individuals who are at risk for disease progression. Furthermore, high levels of alpha IFN may promote autoantibody class-switch from IgM to the more pathogenic IgG class.

Indexed as

Gene Expression RegulationAdultAntibody FormationAutoantibodiesAutoantigensFemaleGene Expression ProfilingHumansImmunoglobulin GImmunoglobulin MInterferonsLupus Erythematosus, SystemicMaleMiddle AgedOligonucleotide Array Sequence AnalysisProteomicsAutoantibodiesAutoantigensImmunoglobulin GImmunoglobulin MInterferons

Identifiers

PMID19968664
PMCPMC2819494
OpenAlexW2073781275

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.