ArticleScience signaling2014
MeCP2 reinforces STAT3 signaling and the generation of effector CD4+ T cells by promoting miR-124-mediated suppression of SOCS5.
Article in Science signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
- Reduced expression of SOCS1-5 and STAT5a genes in Parkinson's disease patients: evidence for dysregulated immune signaling.Molecular biology reports · 2026Article
- microRNA-422a promotes HIV replication and innate immune evasion by targeting MECP2.Molecular therapy. Nucleic acids · 2026Article
- MeCP2 functions as a DNA methylation reader in immune homeostasis and cancer.Frontiers in epigenetics and epigenomics · 2026Review
- Review
- An Irak1-Mecp2 tandem duplication mouse model for the study of MECP2 duplication syndrome.Disease models & mechanisms · 2024Article
- Study of MicroRNA-124 in Patients with Lupus Nephritis.Endocrine, metabolic & immune disorders drug targets · 2024Article
- CircRNAs regulate the crosstalk between inflammation and tumorigenesis: The bilateral association and molecular mechanisms.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- miR-124: A Promising Therapeutic Target for Central Nervous System Injuries and Diseases.Cellular and molecular neurobiology · 2022Review
- STAT3 Role in T-Cell Memory Formation.International journal of molecular sciences · 2022Review
- Genetic susceptibility loci forFrontiers in immunology · 2022Article
- YY1 regulation by miR-124-3p promotes Th17 cell pathogenicity through interaction with T-bet in rheumatoid arthritis.JCI insight · 2021Article
- Prenatal interleukin 6 elevation increases glutamatergic synapse density and disrupts hippocampal connectivity in offspring.Immunity · 2021Article
- Diagnostic Tools and Biomarkers for Severe Drug Eruptions.International journal of molecular sciences · 2021Review
- Tumor-Derived Exosomes Enriched by miRNA-124 Promote Anti-tumor Immune Response in CT-26 Tumor-Bearing Mice.Frontiers in medicine · 2021Article
- Long non‑coding RNA expression profiles identify lncRNA‑XLOC_I2_006631 as a potential novel blood biomarker for Hashimoto's thyroiditis.International journal of molecular medicine · 2020Article
- miR-802 participates in the inflammatory process of inflammatory bowel disease by suppressing SOCS5.Bioscience reports · 2020Article
- Mechanisms of M2 Macrophage-Derived Exosomal Long Non-coding RNA PVT1 in Regulating Th17 Cell Response in Experimental Autoimmune Encephalomyelitisa.Frontiers in immunology · 2020Article
- Duck Tembusu Virus Utilizes miR-221-3p Expression to Facilitate Viral ReplicationFrontiers in microbiology · 2020Article
- Glial Dysfunction in MeCP2 Deficiency Models: Implications for Rett Syndrome.International journal of molecular sciences · 2019Review
- MicroRNA-124 represents a novel diagnostic marker in human lupus nephritis and plays an inhibitory effect on the growth and inflammation of renal mesangial cells by targeting TRAF6.International journal of clinical and experimental pathology · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Methyl CpG binding protein 2 (MeCP2) is an X-linked, multifunctional epigenetic regulator that is best known for its role in the neurological disorder Rett syndrome; however, it is also linked to multiple autoimmune disorders. We examined a potential role for MeCP2 in regulating the responses of CD4+ T cells to stimulation with antigen. MeCP2 was indispensable for the differentiation of naïve CD4+ T cells into T helper type 1 (T(H)1) and T(H)17 cells and for T(H)1- or T(H)17-mediated pathologies in vitro and in vivo. Loss of MeCP2 in CD4+ T cells impaired the expression of the microRNA (miR) miR-124 and consequently relieved miR-124-mediated repression of the translation of suppressor of cytokine signaling 5 (Socs5) mRNA. The resulting accumulation of SOCS5 inhibited the cytokine-dependent activation of signal transducer and activator of transcription 1 (STAT1) and STAT3, which are necessary for the differentiation of T(H)1 and T(H)17 cells, respectively. Upon silencing of MeCP2, primary neurons and astrocytes also failed to respond properly to STAT3-dependent signaling stimulated by neurotrophic factors. Together, these findings suggest that the regulation of STAT3 signaling may represent a common etiology underpinning the roles of MeCP2 in both the nervous and immune systems.
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