Total glucosides of paeony inhibits the differentiation and migration of intestinal mucosal immune Th17 cells in Sjogren’s syndrome mice
- 1School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University
Abstract
Background: Sjogren’s syndrome (SS) is marked by exocrine-gland infiltration and Th17-driven inflammation; low-bioavailability Total glucosides of paeony (TGP) shows efficacy yet unclear mechanisms.
Purpose: To investigate the role of intestinal mucosal immunity in SS pathogenesis and the effect of TGP on the differentiation and migration of Th17 in intestinal mucosal immunity.
Methods: SS was induced in Peyer’s patches (PPs)/mesenteric lymph nodes (MLNs)-deficient mice. Saliva/tear flow, gland histopathology, Th17-related cytokine mRNA and blood Th17 were assessed. Established SS mice were treated with 6-week TGP. Flow cytometry/RT-qPCR evaluated CD4 ⁺ T cell proliferation, dendritic cell (DC) activation, and Th17 differentiation, migration and homing in intestinal mucosal immunity, blood, exocrine glands. Immunofluorescence observed the migration of in vitro -polarized, CFSE-labeled Th17 cells to the submandibular glands (SMG). In vitro , naive CD4 ⁺ T cells from PPs/MLNs were cultured with cytokines or LPS-activated bone marrow DCs (BMDCs) to induce Th17 differentiation, with TGP incubated. CD4 ⁺ T cell proliferation, Th17 proportion and cytokine mRNA was determined.
Results: PPs- or MLNs-deficient SS mice showed no significant increase in SS manifestations or Th17 markers. In vivo , TGP inhibited CD4 ⁺ T cell proliferation, Th17 differentiation and DC activation/migration, blocking Th17 gland entry and gut homing by down-regulating CCR6/CCL20, CCR9/CCL25 and α4β7/MAdCAM-1 axis. Immunofluorescence results also clearly demonstrated that TGP significantly inhibited the migration of intestinal mucosa-derived Th17 cells to the SMG. In vitro , TGP left BMDC activation intact but sharply suppressed BMDC-driven Th17 differentiation by reducing proliferation and Th17 cytokines.
Conclusion: TGP attenuates SS inflammation by inhibiting Th17 differentiation and migration from intestinal mucosal immunity to exocrine glands and their homing to intestinal mucosa.
Related
- Fisetin Induces Apoptosis and Inhibits Migration of Melanoma Cells by Suppressing Glycolytic Metabolism via PKM2 Inhibition.
- MYL9 silencing inhibits proliferation and migration of lung adenocarcinoma cells: a potential therapeutic target.
- HDAC1 inhibits CDX2 expression and promotes colorectal cancer cell migration
- ITGBL1 inhibits obesity and osteoporosis by maintaining adipogenic and osteogenic differentiation balance via the NEDD4–PPARγ–RUNX2 axis
- mTORC1-dependent control of Hedgehog signaling mediates nutrient-responsive licensing of intestinal stem cell differentiation
BibTeX
@article{liu2026total,
title = {{Total glucosides of paeony inhibits the differentiation and migration of intestinal mucosal immune Th17 cells in Sjogren’s syndrome mice}},
author = {Ge Liu and Jing Liu and Xingyu Yan and Teng Chu and Yue Wu and Weirong Fang},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1742485},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1742485/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Total glucosides of paeony inhibits the differentiation and migration of intestinal mucosal immune Th17 cells in Sjogren’s syndrome mice
AU - Ge Liu
AU - Jing Liu
AU - Xingyu Yan
AU - Teng Chu
AU - Yue Wu
AU - Weirong Fang
PY - 2026
DA - 2026/10/13
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1742485
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1742485/full
AB - Background: Sjogren’s syndrome (SS) is marked by exocrine-gland infiltration and Th17-driven inflammation; low-bioavailability Total glucosides of paeony (TGP) shows efficacy yet unclear mechanisms. Purpose: To investigate the role of intestinal mucosal immunity in SS pathogenesis and the effect of TGP on the differentiation and migration of Th17 in intestinal mucosal immunity. Methods: SS was induced in Peyer’s patches (PPs)/mesenteric lymph nodes (MLNs)-deficient mice. Saliva/tear flow, gland histopathology, Th17-related cytokine mRNA and blood Th17 were assessed. Established SS mice were treated with 6-week TGP. Flow cytometry/RT-qPCR evaluated CD4 ⁺ T cell proliferation, dendritic cell (DC) activation, and Th17 differentiation, migration and homing in intestinal mucosal immunity, blood, exocrine glands. Immunofluorescence observed the migration of in vitro -polarized, CFSE-labeled Th17 cells to the submandibular glands (SMG). In vitro , naive CD4 ⁺ T cells from PPs/MLNs were cultured with cytokines or LPS-activated bone marrow DCs (BMDCs) to induce Th17 differentiation, with TGP incubated. CD4 ⁺ T cell proliferation, Th17 proportion and cytokine mRNA was determined. Results: PPs- or MLNs-deficient SS mice showed no significant increase in SS manifestations or Th17 markers. In vivo , TGP inhibited CD4 ⁺ T cell proliferation, Th17 differentiation and DC activation/migration, blocking Th17 gland entry and gut homing by down-regulating CCR6/CCL20, CCR9/CCL25 and α4β7/MAdCAM-1 axis. Immunofluorescence results also clearly demonstrated that TGP significantly inhibited the migration of intestinal mucosa-derived Th17 cells to the SMG. In vitro , TGP left BMDC activation intact but sharply suppressed BMDC-driven Th17 differentiation by reducing proliferation and Th17 cytokines. Conclusion: TGP attenuates SS inflammation by inhibiting Th17 differentiation and migration from intestinal mucosal immunity to exocrine glands and their homing to intestinal mucosa.
SN - 1664-3224
ER -