ArticleFrontiers in immunology2025
Glucocorticoid receptor inhibits Th2 immune responses by down-regulating Pparg and Gata3 in schistosomiasis.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Differential regulation of type 2 immunity by glucocorticoids.BMB reports · 2026Review
- Advances in Single-Cell Sequencing for Infectious Diseases: Progress and Perspectives.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The Th2 immune response plays a pivotal role in the pathogenesis of schistosomiasis, contributing to the formation of hepatic granulomas and fibrosis. While the glucocorticoid receptor (GR) is a ubiquitously expressed nuclear receptor that mediates anti-inflammatory effects, its impact on Th2 responses in schistosomiasis remains underexplored. Thus, this study aimed to investigate the potential impact of GR activation on the hepatic Th2 immune response in schistosomiasis using the synthetic glucocorticoid dexamethasone. Method: Results: Conclusion: GR activation may suppress the Th2 immune response triggered by egg antigens by downregulating the expression of the key transcription factors Gata3 and Pparg. While these findings provide insights into a potential complementary therapeutic strategy, further research is necessary to assess the feasibility and safety of targeting GR activation for the treatment of schistosomiasis.
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