ArticleLaboratory investigation; a journal of technical methods and pathology2015
Inactivation of Notch signaling reverses the Th17/Treg imbalance in cells from patients with immune thrombocytopenia.
Article in Laboratory investigation; a journal of technical methods and pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 64 citations in OpenAlex.
- MLL1 Regulates T-Cell Phenotype via Notch Signaling During Abdominal Aortic Aneurysm Development.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Therapeutic effect of miR-30b-5p-loaded lentivirus on experimental autoimmune uveitis via inhibiting Notch signaling activation.Journal of translational medicine · 2025Article
- The function of T cells in immune thrombocytopenia.Frontiers in immunology · 2025Review
- The histone methyltransferase Mixed-lineage-leukemia-1 drives T cell phenotype via Notch signaling in diabetic tissue repair.JCI insight · 2024Article
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- Resveratrol inhibits AhR/Notch axis and reverses Th17/Treg imbalance in purpura by activating Foxp3.Toxicology research · 2023Article
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- Cellular and molecular mechanisms of Notch signal in pulmonary microvascular endothelial cells after acute lung injury.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023Article
- Significance of NotchScore and JAG1 in predicting prognosis and immune response of low-grade glioma.Frontiers in immunology · 2023Article
- Role of IL-10 and IL-22 cytokines in patients with primary immune thrombocytopenia and their clinical significance.Journal of clinical laboratory analysis · 2022Article
- Intrauterine administration of peripheral blood mononuclear cells (PBMCs) improves embryo implantation in mice by regulating local Treg/Th17 cell balance.The Journal of reproduction and development · 2021Article
- TGF-β-induced CD4+ FoxP3+ regulatory T cell-derived extracellular vesicles modulate Notch1 signaling through miR-449a and prevent collagen-induced arthritis in a murine model.Cellular & molecular immunology · 2021Article
- Regulation of Th1/Th2 and Th17/Treg by pDC/mDC imbalance in primary immune thrombocytopenia.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Predicting bleeding risk in a Chinese immune thrombocytopenia (ITP) population: development and assessment of a new predictive nomogram.Scientific reports · 2020Article
- miR-106b-5p induces immune imbalance of Treg/Th17 in immune thrombocytopenic purpura through NR4A3/Foxp3 pathway.Cell cycle (Georgetown, Tex.) · 2020Article
- The Role of Classical and Novel Forms of Vitamin D in the Pathogenesis and Progression of Nonmelanoma Skin Cancers.Advances in experimental medicine and biology · 2020Review
- Inhibiting the Notch signaling pathway suppresses Th17-associated airway hyperresponsiveness in obese asthmatic mice.Laboratory investigation; a journal of technical methods and pathology · 2019Article
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- Activation of the Notch signaling pathway disturbs the CD4Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T helper 17 (Th17) cells and regulatory T (Treg) cells, along with Th1 and Th2 cells, may contribute to the development of immune thrombocytopenia (ITP). The imbalance of Th17/Treg toward Th17 cells has been shown to play a pivotal role in the peripheral immune response. Notch signaling has been implicated in peripheral T-cell activation and effector cell differentiation. However, the role of Th17/Treg in the pathogenesis of ITP and the effect of Notch signaling on Th17/Treg imbalances remain largely elusive in ITP. In vitro, we treated peripheral blood mononuclear cells (PBMCs) from ITP and healthy controls with γ-secretase inhibitor (DAPT). Th17 cells and Treg cells were measured by flow cytometry and IL-17, IL-21, and IL-10 secretion by enzyme immunoassay technique. The mRNA expression of Ntoch1, Hes1, Hey1, RORγt, and Foxp3 was investigated by RT-PCR. Cell proliferation and apoptosis were determined by the Cell Counting Kit-8 and apoptosis detection kit. We demonstrated that DAPT was effective in inhibiting mRNA expression of Notch signaling molecules. In untreated cultured PBMCs from ITP patients, we observed elevated Th17 cell and IL-21 levels and RORγt mRNA expression, decreased Treg cells and Foxp3 mRNA expression, and an increased ratio of Th17/Treg and RORγt/Foxp3. After inactivating Notch signal by DAPT, Th17 cells and Th17/Treg ratio were dose dependently decreased and accompanied by the reduction of IL-17 in culture supernatants and RORγt mRNA expression in ITP patients. However, no significant difference was found for Treg cells and Foxp3 mRNA expression, RORγt/Foxp3 ratio, and IL-21 and IL-10 levels after DAPT treatment in ITP patients. We also present evidence that the effect of DAPT inhibition on the Th17 cell response was associated with downregulation of RORγt and IL-17 transcription using human in vitro polarization. In conclusion, our findings highlight the importance of Notch signaling in Th17/Treg imbalances in ITP. Inactivation of Notch signaling might be a potential immunoregulatory strategy in ITP patients.
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