ArticleMolecular medicine (Cambridge, Mass.)2024
TWEAK/Fn14 disrupts Th17/Treg balance and aggravates conjunctivitis by inhibiting the Nrf2/HO-1 pathway in allergic conjunctivitis mice.
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Fibroblast growth factor-inducible 14 accelerates pulmonary fibrosis by inducing fibroblast senescence in mice.Cellular and molecular life sciences : CMLS · 2026Article
- Cold Atmospheric Plasma Enhances Fn14 Signaling in Hair Follicle Stem Cells, Thereby Promoting the Healing of Diabetic Skin Wounds in a Mouse Model.Journal of immunology research · 2026Article
- Aurintricarboxylic Acid Attenuates Tramadol Withdrawal Syndrome Via TWEAK/FN14 Inhibition and CREB Modulation in Mice Model.Neuromolecular medicine · 2025Article
- TWEAK-Fn14: a promising target for cardio-cerebrovascular diseases and brain-heart syndrome.Frontiers in immunology · 2025Review
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4 authors.
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Abstract
backgroundAllergic conjunctivitis (AC) affects people's daily life and work, especially the health of children. Although there are few relevant studies, Th17/Treg imbalance plays an important role in AC development. The aim of this study was to elucidate the effect of TWEAK/Fn14 on AC and Th17/Treg balance.
methodsOvalbumin induced AC mouse model was utilized to observe the mechanism of TWEAK/Fn14 in vivo. Conjunctivitis was evaluated by hematoxylin-eosin staining, toluidine blue staining and AC clinical score. Flow cytometry was used to measure Th17 and Treg cell ratios. The level of Th17/Treg balance related factors and Nrf2/HO-1 signal was detected by ELISA, WB, qRT-PCR and immunohistochemistry.
resultsIn the AC state, disruption of Th17/Treg cell balance, increased TWEAK/Fn14 signaling level and conjunctival inflammation were observed. After TWEAK knockdown, Th17 cell differentiation was inhibited, Treg cell differentiation was promoted, and AC symptoms were alleviated in AC mice. Moreover, TWEAK knockdown caused an enhancement of the Nrf2/HO-1 signaling pathway in the AC models. Treatment with Nrf2 inhibitor reversed these changes induced by TWEAK knockdown. Therefore, TWEAK/Fn14 regulated the Nrf2/HO-1 pathway to affect Th17/Treg cell balance and conjunctivitis in AC mouse models.
conclusionIn summary, TWEAK/Fn14 caused Th17/Treg imbalance by inhibiting Nrf2/HO-1 pathway, which might be one potential mechanism of the exacerbation of AC.
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