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Updated: Dec 3, 2025

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
Published on: December 16, 2021
Exosomes derived from T regulatory cells relieve inflammatory bowel disease by transferring miR-195a-3p
Fei Liao1, Xiaohong Lu1, Weiguo Dong1
1Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China.
Previous studies have demonstrated the therapeutic effects of regulatory T (Treg) cells on inflammatory bowel disease (IBD), but the mechanism is not well-understood. Exosomes have been proposed as a novel mechanism underlying the action of Tregs. This study aimed to investigate the therapeutic effects of exosomes secreted by Treg cells (Treg-Exo) on IBD and to explore the underlying mechanism. Treg-Exo was isolated from BALB/c mouse spleen mononuclear cells and then injected into a murine model of IBD induced by dextran sodium sulfate (DSS) exposure. A co-culture model of Treg-Exo and colonic epithelial YAMC cells in the presence of TNF-α was used to investigate the communication between Tregs and intestinal epithelial cells. in vitro results showed that Treg-Exo could be transferred to YAMC cells where Treg-Exo promoted cell proliferation and inhibited cell apoptosis. Animal experiments showed that Treg-Exo administration alleviated the DSS-induced IBD in mice. The therapeutic effects of Treg-Exo both in vitro and in vivo were eliminated when miR-195a-3p expression was inhibited in Treg-Exo. The pro-apoptotic Caspase 12 was identified as a direct target of miR-195a-3p. In conclusion, Treg-Exo alleviated the DSS-induced IBD through transferring miR-195a-3p.
Previous studies have demonstrated the therapeutic effects of regulatory T (Treg) cells on inflammatory bowel disease (IBD), but the mechanism is not well-understood. Exosomes have been proposed as a novel mechanism underlying the action of Tregs. This study aimed to investigate the therapeutic effects of exosomes secreted by Treg cells (Treg-Exo) on IBD and to explore the underlying mechanism. Treg-Exo was isolated from BALB/c mouse spleen mononuclear cells and then injected into a murine model of IBD induced by dextran sodium sulfate (DSS) exposure. A co-culture model of Treg-Exo and colonic epithelial YAMC cells in the presence of TNF-α was used to investigate the communication between Tregs and intestinal epithelial cells. in vitro results showed that Treg-Exo could be transferred to YAMC cells where Treg-Exo promoted cell proliferation and inhibited cell apoptosis. Animal experiments showed that Treg-Exo administration alleviated the DSS-induced IBD in mice. The therapeutic effects of Treg-Exo both in vitro and in vivo were eliminated when miR-195a-3p expression was inhibited in Treg-Exo. The pro-apoptotic Caspase 12 was identified as a direct target of miR-195a-3p. In conclusion, Treg-Exo alleviated the DSS-induced IBD through transferring miR-195a-3p.
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