Trial reportThe Journal of biological chemistry2014
cAMP responsive element modulator (CREM) α mediates chromatin remodeling of CD8 during the generation of CD3+ CD4- CD8- T cells.
Trial report in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 80 citations in OpenAlex.
- CaMK4-dependent activation of AKT/mTOR and CREM-α underlies autoimmunity-associated Th17 imbalance.The Journal of clinical investigation · 2014Trial
- Single-cell transcriptomics reveals heterogeneity and immune microenvironment in lymphatic metastasis of head and neck squamous cell carcinoma.Genes and immunity · 2026Article
- An Update Comprehensive Review on Epigenetic Modifications and Therapies in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2026Review
- Epigenetic Alterations in Microbiome-Host Interactions in Inflammatory and Autoimmune Diseases.International journal of molecular sciences · 2026Review
- REGULATION OF COLONIC MACROPHAGES AND TYPE-17 AND REGULATORY T CELLS IN DSS-COLITIS BY IBD-ASSOCIATED TRANSCRIPTION FACTOR, CREM.bioRxiv : the preprint server for biology · 2026Article
- Unveiling Molecular Mechanisms Underlying Obesity-Associated Systemic Lupus Erythematosus.Endocrinology, diabetes & metabolism · 2025Review
- Article
- Gluconolactone restores immune regulation and alleviates skin inflammation in lupus-prone mice and in patients with cutaneous lupus.Science translational medicine · 2025Article
- Article
- Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025Review
- Article
- Rab4A-directed endosome traffic shapes pro-inflammatory mitochondrial metabolism in T cells via mitophagy, CD98 expression, and kynurenine-sensitive mTOR activation.Nature communications · 2024Article
- CaMK4 controls follicular helper T cell expansion and function during normal and autoimmune T-dependent B cell responses.Nature communications · 2024Article
- Investigating the Heterogeneity of Immune Cells in Triple-Negative Breast Cancer at the Single-Cell Level before and after Paclitaxel Chemotherapy.International journal of molecular sciences · 2023Article
- Glucocorticoid prevents CD138 expression in T cells of autoimmune MRL/Molecular medicine reports · 2022Article
- The Role of Oxidative Stress in Epigenetic Changes Underlying Autoimmunity.Antioxidants & redox signaling · 2022Review
- Cyclic AMP Response Element Modulator-α Suppresses PD-1 Expression and Promotes Effector CD4Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- LangChuangHeJi decoction ameliorates lupus via preventing accumulation of CD138+ T cells in MRL/lpr mice.American journal of translational research · 2021Article
- Fas/FasL Signaling Regulates CD8 Expression During Exposure to Self-Antigens.Frontiers in immunology · 2021Article
- Clinical value of DNA methylation markers in autoimmune rheumatic diseases.Nature reviews. Rheumatology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
TCR-αβ(+)CD3(+)CD4(-)CD8(-) "double negative" T cells are expanded in the peripheral blood of patients with systemic lupus erythematosus (SLE) and lupus-prone mice. Double negative T cells have been claimed to derive from CD8(+) cells that down-regulate CD8 co-receptors and acquire a distinct effector phenotype that includes the expression of proinflammatory cytokines. This, along with the fact that double negative T cells have been documented in inflamed organs, suggests that they may contribute to disease expression and tissue damage. We recently linked the transcription factor cAMP responsive element modulator (CREM) α, which is expressed at increased levels in T cells from SLE patients and lupus prone MRL/lpr mice, with trans-repression of a region syntenic to the murine CD8b promoter. However, the exact molecular mechanisms that result in a stable silencing of both CD8A and CD8B genes remain elusive. Here, we demonstrate that CREMα orchestrates epigenetic remodeling of the CD8 cluster through the recruitment of DNA methyltransferase (DNMT) 3a and histone methyltransferase G9a. Thus, we propose that CREMα is essential for the expansion of double negative T cells in SLE. CREMα blockade may have therapeutic value in autoimmune disorders with DN T cell expansion.
Indexed as
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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.