Article3 Biotech2024
Selective blockade of IL-21 by myricetin impedes T follicular helper cell differentiation by negatively regulating the JAK/STAT/Bcl-6 pathway in a rheumatoid arthritis animal model.
Article in 3 Biotech, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- STING Drives CD4Experimental dermatology · 2026Article
- Myricetin Suppresses Inflammatory Th17 Polarization to Mitigate Alzheimer's Disease Pathogenesis.CNS neuroscience & therapeutics · 2025Article
- JAK Inhibitors in Rheumatoid Arthritis: Immunomodulatory Properties and Clinical Efficacy.International journal of molecular sciences · 2024Review
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5 authors at 1 institution in 1 country.
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Abstract
Interleukin (IL)-21 is a major lineage-defining factor that promotes Tfh cell differentiation. The current study investigated the molecular basis of myricetin, a flavonoid that impedes IL-21-mediated differentiation of Tfh cells in RA. Through high-throughput virtual screening of natural compounds that inhibit IL-21, we found that myricetin binds to IL-21 and hampers its interaction with IL-21 receptor (IL-21R). Our in vivo studies demonstrated that myricetin treatment ameliorated the clinical manifestations in adjuvant-induced arthritis (AIA) mice by reducing paw thickness and cellular infiltration. In addition, myricetin inhibited splenic Tfh cell differentiation and IL-21 production in AIA mice. Myricetin negatively regulates JAK/STAT signaling and the downstream Bcl-6 transcription factor at the molecular level, which arrests Tfh cell differentiation. Our current research proposal to target IL-21 with myricetin inevitably represents a new molecular approach that expedites new alternative drugs for rheumatoid arthritis therapy. Supplementary Information: The online version contains supplementary material available at 10.1007/s13205-023-03880-w.
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