| First Author | Wu C | Year | 2014 |
| Journal | Immunity | Volume | 41 |
| Issue | 2 | Pages | 270-82 |
| PubMed ID | 25065622 | Mgi Jnum | J:224716 |
| Mgi Id | MGI:5688819 | Doi | 10.1016/j.immuni.2014.06.011 |
| Citation | Wu C, et al. (2014) Galectin-9-CD44 interaction enhances stability and function of adaptive regulatory T cells. Immunity 41(2):270-82 |
| abstractText | The beta-galactoside-binding protein galectin-9 is critical in regulating the immune response, but the mechanism by which it functions remains unclear. We have demonstrated that galectin-9 is highly expressed by induced regulatory T cells (iTreg) and was crucial for the generation and function of iTreg cells, but not natural regulatory T (nTreg) cells. Galectin-9 expression within iTreg cells was driven by the transcription factor Smad3, forming a feed-forward loop, which further promoted Foxp3 expression. Galectin-9 increased iTreg cell stability and function by directly binding to its receptor CD44, which formed a complex with transforming growth factor-beta (TGF-beta) receptor I (TGF-betaRI), and activated Smad3. Galectin-9 signaling was further found to regulate iTreg cell induction by dominantly acting through the CNS1 region of the Foxp3 locus. Our data suggest that exogenous galectin-9, in addition to being an effector molecule for Treg cells, acts synergistically with TGF-beta to enforce iTreg cell differentiation and maintenance. |
