ArticleLupus2011
A systemic lupus erythematosus gene expression array in disease diagnosis and classification: a preliminary report.
Article in Lupus, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Spleen tyrosine kinase (Syk) regulates systemic lupus erythematosus (SLE) T cell signaling.PloS one · 2013Trial
- Comparison of Role of Hand and Wrist Ultrasound in Diagnosis of Subclinical Synovitis in Patients with Systemic Lupus Erythematosus and Rheumatoid Arthritis: A Retrospective, Single-Center Study.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- SLAMF6 clustering is required to augment T cell activation.PloS one · 2019Article
- New insights into the immunopathogenesis of systemic lupus erythematosus.Nature reviews. Rheumatology · 2016Review
- A T cell gene expression panel for the diagnosis and monitoring of disease activity in patients with systemic lupus erythematosus.Clinical immunology (Orlando, Fla.) · 2014Article
- Systemic lupus erythematosus diagnostics in the 'omics' era.International journal of clinical rheumatology · 2013Article
- Biomarkers in systemic lupus erythematosus: challenges and prospects for the future.Therapeutic advances in musculoskeletal disease · 2013Article
- Abnormalities of T cell signaling in systemic lupus erythematosus.Arthritis research & therapy · 2011Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a clinically heterogeneous disease diagnosed on the presence of a constellation of clinical and laboratory findings. At the pathogenetic level, multiple factors using diverse biochemical and molecular pathways have been recognized. Succinct recognition and classification of clinical disease subsets, as well as the availability of disease biomarkers, remains largely unsolved. Based on information produced by the present authors' and other laboratories, a lupus gene expression array consisting of 30 genes, previously claimed to contribute to aberrant function of T cells, was developed. An additional eight genes were included as controls. Peripheral blood was obtained from 10 patients (19 samples) with SLE and six patients with rheumatoid arthritis (RA) as well as 19 healthy controls. T cell mRNA was subjected to reverse transcription and PCR, and the gene expression levels were measured. Conventional statistical analysis was performed along with principal component analysis (PCA) to capture the contribution of all genes to disease diagnosis and clinical parameters. The lupus gene expression array faithfully informed on the expression levels of genes. The recorded changes in expression reflect those reported in the literature by using a relatively small (5 ml) amount of peripheral blood. PCA of gene expression levels placed SLE samples apart from normal and RA samples regardless of disease activity. Individual principal components tended to define specific disease manifestations such as arthritis and proteinuria. Thus, a lupus gene expression array based on genes previously claimed to contribute to immune pathogenesis of SLE may define the disease, and principal components of the expression of 30 genes may define patients with specific disease manifestations.
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Registered trials
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.