ArticleFrontiers in immunology2022
Parthenolide Suppresses T Helper 17 and Alleviates Experimental Autoimmune Encephalomyelitis.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Review
- Neuronal inflammasomes: balancing immunity, neuroinflammation, and homeostasis.Trends in immunology · 2026Review
- Morroniside ameliorates experimental autoimmune encephalomyelitis by regulating gut microenvironment, immune balance, and NF-κB neuroinflammatory pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- NLRP3 inflammasome in neuroinflammation and central nervous system diseases.Cellular & molecular immunology · 2025Review
- Inflammasomes in neurodegenerative diseases.Translational neurodegeneration · 2024Review
- A Comparison between BulgarianMolecules (Basel, Switzerland) · 2024Article
- Th17-Gene Expression Profile in Patients with Chronic Venous Disease and Venous Ulcers: Genetic Modulations and Preliminary Clinical Evidence.Biomolecules · 2022Article
- Article
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T helper (Th) cells play crucial roles in inflammation and adaptive immune system. Importantly, Th17 cells, a major pathogenic Th cell subset, are involved in the pathogenesis of multiple sclerosis (MS) and its classical animal modal experimental autoimmune encephalomyelitis (EAE). Previous studies have shown that parthenolide (PTL), a sesquiterpene lactone, possesses potent anti-cancer and anti-inflammatory activities. However, the immunosuppressive effect of PTL on the pathogenic Th17 cell and MS is unclear. In this study, we showed that PTL treatment could alleviate clinical symptoms by inhibiting inflammatory cell infiltration, reducing inflammation and demyelination of CNS. In addition, the mRNA expression of cytokines and inflammatory factors in CD4
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