ArticleFrontiers in immunology2025
Cigarette smoke exposure triggers dendritic cell-derived exosome-mediated Th17 and Treg polarization through an autophagy- and necroptosis-associated SIRT1-dependent mechanism in vitro.
Article in Frontiers in immunology, 2025. 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.
- Mitochondrial dysfunction and the regulatory cell death crosstalk network in chronic obstructive pulmonary disease: from oxidative stress mechanisms to targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Epitranscriptomics, immunometabolism, and NETosis: unlocking novel mechanisms of traditional Chinese medicine in COPD.Frontiers in immunology · 2026Review
- The role of programmed cell death in chronic obstructive pulmonary disease: from pathogenesis to treatment.Frontiers in immunology · 2026Review
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Authors and funding
9 authors.
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Abstract
Introduction: Both Th17/Treg cell imbalance and dendritic cells (DCs) play critical roles in chronic obstructive pulmonary disease pathogenesis from cigarette smoke. Previous studies have shown that DC-derived exosomes (DCexos) can polarize CD4 Methods: DCs were generated from bone marrow-derived mononuclear cells isolated from C57BL/6J mice and assigned to three groups: control DCs, CSE-exposed DCs, and SRT1720-treated CSE-exposed DCs. The ability of each group's exosomes to polarize CD4 Results: SIRT1 expression in CSE-exposed DCs decreased in a time-dependent manner (all Conclusion: CSE exposure induces an imbalance in Th17/Treg polarization through a process mediated by DCexos that entails reduced SIRT1 expression, increased necroptosis, and dysregulated autophagy. SIRT1 activation by SRT1720 can attenuate these effects by restoring immune balance and modulating cell death and survival pathways in DCs under CSE exposure.
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