Restoring Immune Balance in Allergic Airway Inflammation: Yanghe Pingchuan Granules Regulate Th17/Treg via PD-1/PD-L1 Pathway.
[INTRODUCTION] Allergic airway inflammation (AAI), an asthma-like condition, is characterized by Th17/Treg imbalance and PD-1/PD-L1 pathway dysregulation.
APA
Yang L, Li X, et al. (2026). Restoring Immune Balance in Allergic Airway Inflammation: Yanghe Pingchuan Granules Regulate Th17/Treg via PD-1/PD-L1 Pathway.. Combinatorial chemistry & high throughput screening. https://doi.org/10.2174/0113862073412055251107212524
MLA
Yang L, et al.. "Restoring Immune Balance in Allergic Airway Inflammation: Yanghe Pingchuan Granules Regulate Th17/Treg via PD-1/PD-L1 Pathway.." Combinatorial chemistry & high throughput screening, 2026.
PMID
41568494
Abstract
[INTRODUCTION] Allergic airway inflammation (AAI), an asthma-like condition, is characterized by Th17/Treg imbalance and PD-1/PD-L1 pathway dysregulation. Yanghe Pingchuan Granules (YP) formulation is clinically used to treat asthma, but its immunomodulatory mechanisms remain unclear.
[METHODS] Using an AAI rat model, the effects of YP were assessed. Flow cytometry was carried out to analyze Th17/Treg proportions. Additionally, the expression levels of Foxp3, ROR?t, IL- 10, IL-17, and TGF-1 were measured. PD-L1 siRNA knockdown and overexpression studies were performed to elucidate the role of the pathway.
[RESULTS] YP treatment restored the Th17/Treg balance by reducing Th17 and increasing Treg cells. It upregulated IL-10 and TGF-1 while downregulating IL-17. YP inhibited the PD-1/PDL1 pathway, correlating with improved immune balance and reduced inflammation. PD-L1 modulation confirmed its role in mediating the effects of YP on cellular and cytokine profiles.
[DISCUSSION] The findings indicated that the therapeutic action of YP involves modulation of the Th17/Treg imbalance, likely through inhibition of the PD-1/PD-L1 pathway, thereby shifting thecytokine milieu from a pro- to an anti-inflammatory state.
[CONCLUSION] YP alleviates AAI by modulating the PD-1/PD-L1 pathway to restore Th17/Treg balance and suppress inflammation, thereby revealing its potential immunomodulatory mechanism.
[METHODS] Using an AAI rat model, the effects of YP were assessed. Flow cytometry was carried out to analyze Th17/Treg proportions. Additionally, the expression levels of Foxp3, ROR?t, IL- 10, IL-17, and TGF-1 were measured. PD-L1 siRNA knockdown and overexpression studies were performed to elucidate the role of the pathway.
[RESULTS] YP treatment restored the Th17/Treg balance by reducing Th17 and increasing Treg cells. It upregulated IL-10 and TGF-1 while downregulating IL-17. YP inhibited the PD-1/PDL1 pathway, correlating with improved immune balance and reduced inflammation. PD-L1 modulation confirmed its role in mediating the effects of YP on cellular and cytokine profiles.
[DISCUSSION] The findings indicated that the therapeutic action of YP involves modulation of the Th17/Treg imbalance, likely through inhibition of the PD-1/PD-L1 pathway, thereby shifting thecytokine milieu from a pro- to an anti-inflammatory state.
[CONCLUSION] YP alleviates AAI by modulating the PD-1/PD-L1 pathway to restore Th17/Treg balance and suppress inflammation, thereby revealing its potential immunomodulatory mechanism.
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