ArticleFrontiers in immunology2026
Modified Guilu Erxian Glue restores immune tolerance in aplastic anemia by reprogramming T cell differentiation via the miR-146a/STAT1/SOCS1 axis.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Two traditional Chinese medicine (TCM) formulas are Guilu Erxian Glue (GEG) and Danggui Buxue Tang (DBT). Their combination, Modified Guilu Erxian Glue (MGEG), is used to treat aplastic anemia (AA). This study aims to clarify how MGEG restores immune tolerance in AA mice. Specifically, we studied whether MGEG can regulate the differentiation and maturation of T cell lineage by regulating the transcription of miR-146a to rebuild the stable state of bone marrow immune microenvironment, inhibit the immune response mediated by T helper (Th)1 cells, and enhance the immunosuppressive function of regulatory T cells (Tregs). Materials and methods: MGEG's active constituents and potential targets were identified using HPLC-ESI-MS and network pharmacology. Sublethal irradiation and immune cell infusion were used to create an AA mouse model. Bone marrow histopathology and peripheral blood parameters were used to assess therapeutic efficacy. T cell subsets and the maturation phenotypes of naïve/effector memory T cells were thoroughly examined using mass cytometry (CyTOF) and flow cytometry. ELISA was used to measure cytokine levels associated with T cell subsets and apoptosis. qPCR quantified miR-146a and its target gene, STAT1, expression levels. The expression levels of important proteins in the STAT1/SOCS1, Fas/FasL, and IL-2/STAT5 signaling pathways as well as lineage-defining transcription factors (T-bet, Foxp3, RORγ, GATA3) were assessed using Western blot. Results: Network pharmacology indicated MGEG primarily modulates JAK-STAT and apoptosis pathways. Conclusion: MGEG treats AA by constructing a multi-dimensional immunomodulatory network: it suppresses Th1-mediated inflammation via the miR-146a/STAT1/SOCS1 axis, preserves Treg function through the IL-2/STAT5 and Fas/FasL pathways, and corrects the imbalance between naïve and Tem cells, maintaining long-term immune reserve and homeostasis.
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