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Updated: Mar 15, 2026

In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction
Published on: January 22, 2020
Oleic Acid Promotes Treg Cell Differentiation via Autophagy Induction and Ameliorates DSS-Induced Colitis
Minghui Xia1,2, Yang Liu3, Xiujuan Zhao4
1Department of Laboratory Medicine, Wuhan No.1 Hospital, Wuhan, Hubei, China.
Oleic acid (OA) promotes T regulatory cell (Treg) differentiation, crucial for ulcerative colitis (UC) treatment. This dietary fatty acid enhances autophagy, reducing inflammation and disease severity in colitis models.
Area of Science:
- Immunology
- Gastroenterology
- Nutrition Science
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease.
- Oleic acid (OA), abundant in olive oil, has shown anti-inflammatory potential in UC.
- The precise immunomodulatory mechanisms of OA in UC remain unclear.
Purpose of the Study:
- To investigate the immunomodulatory effects of oleic acid (OA) on T regulatory cell (Treg) differentiation.
- To elucidate the role of autophagy in OA-mediated Treg induction.
- To evaluate the therapeutic potential of OA in a preclinical model of colitis.
Main Methods:
- In vitro studies assessing Treg differentiation in response to OA.
- Analysis of mTORC1 and AMPK signaling pathways and their impact on autophagy.
- In vivo experiments using a dextran sulfate sodium (DSS)-induced colitis model in mice.
Main Results:
- OA dose-dependently promoted T regulatory cell (Treg) differentiation.
- OA inhibited mTORC1 signaling and activated AMPK, enhancing autophagy.
- Autophagy blockade abolished OA-induced Treg differentiation.
- OA administration reduced colitis severity, increasing Treg populations in the colon.
Conclusions:
- Oleic acid (OA) promotes Treg differentiation through an autophagy-dependent mechanism.
- OA ameliorates DSS-induced colitis, suggesting its therapeutic potential for UC.
- Dietary intake of OA may serve as a beneficial supplementary therapy for ulcerative colitis.
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