Trial reportThe Journal of biological chemistry2013
cAMP-responsive element modulator α (CREMα) trans-represses the transmembrane glycoprotein CD8 and contributes to the generation of CD3+CD4-CD8- T cells in health and disease.
Trial report in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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.
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
29 citing papers in PubMed, 61 citations in OpenAlex.
- cAMP responsive element modulator (CREM) α mediates chromatin remodeling of CD8 during the generation of CD3+ CD4- CD8- T cells.The Journal of biological chemistry · 2014Trial
- A pan-cancer single cell landscape reveals heterogeneity and functional diversity of double-negative T cells.Molecular cancer · 2026Article
- Two-Sample Bidirectional Mendelian Randomization Analysis of the Causal Relationship Between Immune Cell Phenotypes and Systemic Lupus Erythematosus.Clinical, cosmetic and investigational dermatology · 2026Article
- Gluconolactone restores immune regulation and alleviates skin inflammation in lupus-prone mice and in patients with cutaneous lupus.Science translational medicine · 2025Article
- Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025Review
- Cell type-specific mechanistic target of rapamycin-dependent distortion of autophagy pathways in lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022Review
- Glucocorticoid prevents CD138 expression in T cells of autoimmune MRL/Molecular medicine reports · 2022Article
- Application of double-negative T cells in haematological malignancies: recent progress and future directions.Biomarker research · 2022Review
- Establishing Reference Values for Peripheral Blood Lymphocyte Subsets of Healthy Children in China Using a Single Platform.Journal of immunology research · 2022Article
- Cyclic AMP Response Element Modulator-α Suppresses PD-1 Expression and Promotes Effector CD4Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- T Cell Abnormalities in the Pathogenesis of Systemic Lupus Erythematosus: an Update.Current rheumatology reports · 2021Review
- LangChuangHeJi decoction ameliorates lupus via preventing accumulation of CD138+ T cells in MRL/lpr mice.American journal of translational research · 2021Article
- TCR-α/β CD4Journal of leukocyte biology · 2020Article
- Autoimmunity and organ damage in systemic lupus erythematosus.Nature immunology · 2020Review
- Current Insights and Future Prospects for Targeting IL-17 to Treat Patients With Systemic Lupus Erythematosus.Frontiers in immunology · 2020Review
- Double-negative T cells remarkably promote neuroinflammation after ischemic stroke.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- T cells and IL-17 in lupus nephritis.Clinical immunology (Orlando, Fla.) · 2017Review
- Epigenetics in SLE.Current rheumatology reports · 2017Review
- T cells and autoimmune kidney disease.Nature reviews. Nephrology · 2017Review
- DNA methylation in systemic lupus erythematosus.Epigenomics · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
T cell receptor-αβ(+) CD3(+)CD4(-)CD8(-) "double-negative" T cells are expanded in the peripheral blood of patients with systemic lupus erythematosus and autoimmune lymphoproliferative syndrome. In both disorders, double-negative T cells infiltrate tissues, induce immunoglobulin production, and secrete proinflammatory cytokines. Double-negative T cells derive from CD8(+) T cells through down-regulation of CD8 surface co-receptors. However, the molecular mechanisms orchestrating this process remain unclear. Here, we demonstrate that the transcription factor cAMP-responsive element modulator α (CREMα), which is expressed at increased levels in T cells from systemic lupus erythematosus patients, contributes to transcriptional silencing of CD8A and CD8B. We provide the first evidence that CREMα trans-represses a regulatory element 5' of the CD8B gene. Therefore, CREMα represents a promising candidate in the search for biomarkers and treatment options in diseases in which double-negative T cells contribute to the pathogenesis.
Indexed as
Identifiers
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.