ArticleThe Journal of biological chemistry2011
cAMP-responsive element modulator (CREM)α protein induces interleukin 17A expression and mediates epigenetic alterations at the interleukin-17A gene locus in patients with systemic lupus erythematosus.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed.
- CaMK4-dependent activation of AKT/mTOR and CREM-α underlies autoimmunity-associated Th17 imbalance.The Journal of clinical investigation · 2014Trial
- 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
- 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.The Journal of biological chemistry · 2013Trial
- cAMP-responsive element modulator α (CREMα) suppresses IL-17F protein expression in T lymphocytes from patients with systemic lupus erythematosus (SLE).The Journal of biological chemistry · 2012Trial
- 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
- EPHX1 enhances drug resistance to regorafenib by activating the JAK/STAT signaling pathway in hepatocellular carcinoma cell lines.Hereditas · 2025Article
- Article
- Changes of Peripheral T Cells in Systemic Lupus Erythematosus Patients.Immunity, inflammation and disease · 2025Article
- Towards precision medicine for systemic lupus erythematosus and neuropsychiatric manifestations.Expert review of precision medicine and drug development · 2025Article
- Targeting pro-inflammatory T cells as a novel therapeutic approach to potentially resolve atherosclerosis in humans.Cell research · 2024Article
- Epigenetic Dysregulation in the Pathogenesis of Systemic Lupus Erythematosus.International journal of molecular sciences · 2024Review
- Dissecting the Immune System through Gene Regulation.Advances in experimental medicine and biology · 2024Article
- Kruppel-like factor 2+ CD4 T cells avert microbiota-induced intestinal inflammation.Cell reports · 2023Article
- Article
- The genetically predicted causal relationship of inflammatory bowel disease with bone mineral density and osteoporosis: evidence from two-sample Mendelian randomization.Frontiers in immunology · 2023Article
- Decreased SUV39H1 at the promoter region leads to increased CREMα and accelerates autoimmune response in CD4Clinical epigenetics · 2022Article
- Extracellular adenosine induces hypersecretion of IL-17A by T-helper 17 cells through the adenosine A2a receptor.Brain, behavior, & immunity - health · 2022Article
- Abnormal expression of histone acetylases in CD8+ T cells of patients with severe aplastic anemia.Journal of clinical laboratory analysis · 2022Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors.
Funding
Abstract
IL-17A is a proinflammatory cytokine that is produced by specialized T helper cells and contributes to the development of several autoimmune diseases such as systemic lupus erythematosus (SLE). Transcription factor cAMP-responsive element modulator (CREM)α displays increased expression levels in T cells from SLE patients and has been described to account for aberrant T cell function in SLE pathogenesis. In this report, we provide evidence that CREMα physically binds to a cAMP-responsive element, CRE (-111/-104), within the proximal human IL17A promoter and increases its activity. Chromatin immunoprecipitation assays reveal that activated naïve CD4(+) T cells as well as T cells from SLE patients display increased CREMα binding to this site compared with T cells from healthy controls. The histone H3 modification pattern at the CRE site (-111/-104) and neighboring conserved noncoding sequences within the human IL17A gene locus suggests an accessible chromatin structure (H3K27 hypomethylation/H3K18 hyperacetylation) in activated naïve CD4(+) T cells and SLE T cells. H3K27 hypomethylation is accompanied by decreased cytosine phosphate guanosine (CpG)-DNA methylation in these regions in SLE T cells. Decreased recruitment of histone deacetylase (HDAC)1 and DNA methyltransferase (DNMT)3a to the CRE site (-111/-104) probably accounts for the observed epigenetic alterations. Reporter studies confirmed that DNA methylation of the IL17A promoter indeed abrogates its inducibility. Our findings demonstrate an extended role for CREMα in the immunopathogenesis of SLE because it contributes to increased expression of IL-17A.
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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.