ReviewAnnals of the rheumatic diseases2007
Systemic lupus erythematosus: new molecular targets.
Review in Annals of the rheumatic diseases, 2007. 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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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.
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.
Who cites it
8 citing papers in PubMed.
- From Genes to Pathways: The Molecular Landscape of Systemic Lupus Erythematosus.International journal of molecular sciences · 2026Review
- [Regulatory T-cells in systemic lupus erythematosus. IL-2 is decisive for loss of tolerance].Zeitschrift fur Rheumatologie · 2016Review
- BAFF- and APRIL-targeted therapy in systemic autoimmune diseases.Inflammation and regeneration · 2016Review
- Genetic association of CD247 (CD3ζ) with SLE in a large-scale multiethnic study.Genes and immunity · 2015Article
- The catalytic subunit of protein phosphatase 2A (PP2Ac) promotes DNA hypomethylation by suppressing the phosphorylated mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase (MEK)/phosphorylated ERK/DNMT1 protein pathway in T-cells from controls and systemic lupus erythematosus patients.The Journal of biological chemistry · 2013Article
- Inflammatory cytokines in systemic lupus erythematosus.Journal of biomedicine & biotechnology · 2011Review
- Article
- T cell receptor signaling induced by an analog peptide of type II collagen requires activation of Syk.Clinical immunology (Orlando, Fla.) · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
T cells from patients with systemic lupus erythematosus exhibit a notable array of defects that probably contribute to the origin and development of the disease. Such abnormalities include an abnormal response to stimulation, aberrant expression of molecules that play key roles in intracellular signalling pathways, altered transcription factor activation and binding, and skewed gene expression. The combination of these alterations leads the cell to the expression of a particular phenotype that intense research has gradually uncovered over the last years. The aim of this article is to review the findings that have allowed us to better understand the behaviour of the lupus T cell and highlight the molecules that represent potential therapeutic targets.
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What OpenQuestion holds
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.