ArticleFEBS open bio2013
Tannic acid, a higher galloylated pentagalloylglucose, suppresses antigen-specific IgE production by inhibiting ɛ germline transcription induced by STAT6 activation.
Article in FEBS open bio, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Hydrolyzable Tannins in the Management of Th1, Th2 and Th17 Inflammatory-Related Diseases.Molecules (Basel, Switzerland) · 2022Review
- Unveiling the Ability of Witch Hazel (International journal of molecular sciences · 2022Article
- Co-Application with Tannic Acid Prevents Transdermal Sensitization to Ovalbumin in Mice.International journal of molecular sciences · 2022Article
- Tertiary lymphoid structure related B-cell IgE isotype switching and secondary lymphoid organ linked IgE production in mouse allergy model.BMC immunology · 2020Article
- Pentagalloyl Glucose and Its Functional Role in Vascular Health: Biomechanics and Drug-Delivery Characteristics.Annals of biomedical engineering · 2019Review
- Inhibitory effect of Moutan Cortex aqueous fraction on mast cell-mediated allergic inflammation.Journal of natural medicines · 2015Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-4 is a critical stimulator that induces ɛ germline transcripts (ɛGT) for switch recombination to initiate immunoglobulin (Ig) E and is important in allergic disease pathogenesis. We found pentagalloylglucose (PGG) inhibited IL-4-induced ɛGT expression. PGG exerted its inhibitory function by suppressing IL-4-induced activation of IL-4Rα, JAK3 and STAT6. Furthermore, tannic acid, a higher galloylated PGG, attenuated ovalbumin-induced IgE production in vivo by inhibiting IL-4-induced ɛGT expression and the IL-4 signaling pathway. In conclusion, our results suggest that tannic acid may attenuate allergic diseases by suppressing IgE production by inhibiting IL-4-induced signaling.
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Registered trials
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