| First Author | Ren W | Year | 2019 |
| Journal | Mucosal Immunol | Volume | 12 |
| Issue | 2 | Pages | 531-544 |
| PubMed ID | 30523310 | Mgi Jnum | J:295568 |
| Mgi Id | MGI:6453974 | Doi | 10.1038/s41385-018-0111-7 |
| Citation | Ren W, et al. (2019) Slc6a13 deficiency promotes Th17 responses during intestinal bacterial infection. Mucosal Immunol 12(2):531-544 |
| abstractText | The gamma-amino butyric acid (GABA)ergic system shapes the activation and function of immune cells. The present study was conducted to explore the regulation of GABA transporter (GAT)-2 on the differentiation of Th17 cells. Here we found that Th17 cells show higher abundance of GAT-2, and have distinct cellular metabolic signatures, such as the GABA shunt pathway, as compared to naive T cells. GAT-2 deficiency had little effect on the metabolic signature in naive T cells, but impaired the GABA uptake and GABA shunt pathway in Th17 cells. GAT-2 deficiency had little effect on T cell development and peripheral T cell homeostasis; however, its deficiency promoted Th17 cell differentiation in vitro. Mechanistically, GAT-2 deficiency promoted differentiation of Th17 cells through activation of GABA-mTOR signaling. In a mouse model of intestinal infection and inflammation, GAT-2 deficiency promoted Th17 responses. Collectively, GAT-2 deficiency promotes Th17 cell responses through activation of GABA-mTOR signaling. |
