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熊果酸通过 STAT3/RORγt 通路抑制 Th17 细胞分化，并通过降低 CXCL9/10 的表达抑制雪旺细胞介导的 Th17 细胞迁移。

Ursolic acid inhibits Th17 cell differentiation via STAT3/RORγt pathway and suppresses Schwann cell-mediated Th17 cell migration by reducing CXCL9/10 expression.

机构信息

Department of Neurology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan 250014, Shandong, China.

Department of Neurology, 230965Taian City Central Hospital, Taian 271000, Shandong, China.

出版信息

Innate Immun. 2022 Jul;28(5):155-163. doi: 10.1177/17534259221094559. Epub 2022 May 12.

DOI:10.1177/17534259221094559
PMID:35548957
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9189552/
Abstract

Th17 cells represent important immune cells. Ursolic acid (UA) can regulate immune cell activities. This study was aimed to explore the effects of UA on Th17 cell differentiation and Schwann cell(SCs)-mediated migration and the potential mechanism. Naïve CD4 T cells were isolated from rat peripheral blood, induced for Th17 cell differentiation, and treated with UA. The proportion of Th17 cells was detected by flow cytometry assay. SCs were co-cultured with Th17 cells. Th17 cell migration was detected by Transwell assay. The molecule expression was determined by Western blot and qRT-PCR. UA inhibited the Th17 cell differentiation and suppressed the STAT3/RORγt pathway. STAT3 overexpression up-regulated p-STAT3 and RORγt expression and promoted Th17 cell differentiation under the UA treatment. In LPS- and IFN-γ-stimulated-SCs, UA suppressed the expression of chemokines CXCL9/10, but had no significant effect of CCL20 expression. The expression CXCL9/10 receptor CXCR3 was higher in Th17 cells than that in Treg cells, while the expression CCL20 receptor CCR6 was lower in Th17 cells than that in Treg cells. UA, anti-CXCR3, and anti-CCR6 treatment inhibited SCs-mediated Th17 cell migration, and anti-CXCR3 exerted stronger inhibitory effect than Anti-CCR6. UA inhibited Th17 cell differentiation through STAT3/RORγt pathway and suppressed Th17 cell migration through down-regulating CXCL9/10 expression in SCs.

摘要

辅助性 T 细胞 17（Th17 细胞）是一类重要的免疫细胞，熊果酸（UA）能够调节免疫细胞的活性。本研究旨在探讨 UA 对 Th17 细胞分化及施万细胞（SCs）介导的迁移的影响及其潜在机制。分离大鼠外周血中的初始 CD4+T 细胞，诱导其向 Th17 细胞分化，用 UA 处理。采用流式细胞术检测 Th17 细胞的比例。将 Th17 细胞与 SCs 共培养，采用 Transwell 检测 Th17 细胞的迁移。Western blot 和 qRT-PCR 检测分子表达。UA 抑制 Th17 细胞分化，并抑制 STAT3/RORγt 通路。STAT3 过表达上调 p-STAT3 和 RORγt 的表达，并促进 UA 处理下 Th17 细胞的分化。在 LPS 和 IFN-γ 刺激的 SCs 中，UA 抑制趋化因子 CXCL9/10 的表达，但对 CCL20 的表达无显著影响。Th17 细胞中 CXCL9/10 受体 CXCR3 的表达高于 Treg 细胞，而 Th17 细胞中 CCL20 受体 CCR6 的表达低于 Treg 细胞。UA、抗-CXCR3 和抗-CCR6 处理抑制了 SCs 介导的 Th17 细胞迁移，且抗-CXCR3 发挥的抑制作用强于抗-CCR6。UA 通过 STAT3/RORγt 通路抑制 Th17 细胞分化，并通过下调 SCs 中 CXCL9/10 的表达抑制 Th17 细胞迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c8/9189552/f2c1bcf17fa0/10.1177_17534259221094559-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c8/9189552/ec1a91060fd8/10.1177_17534259221094559-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c8/9189552/36e02f9c8f18/10.1177_17534259221094559-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c8/9189552/c94272170a3c/10.1177_17534259221094559-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c8/9189552/f2c1bcf17fa0/10.1177_17534259221094559-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c8/9189552/ec1a91060fd8/10.1177_17534259221094559-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c8/9189552/36e02f9c8f18/10.1177_17534259221094559-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c8/9189552/c94272170a3c/10.1177_17534259221094559-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c8/9189552/f2c1bcf17fa0/10.1177_17534259221094559-fig4.jpg

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