| First Author | Lee HM | Year | 2015 |
| Journal | PLoS Pathog | Volume | 11 |
| Issue | 2 | Pages | e1004635 |
| PubMed ID | 25658840 | Mgi Jnum | J:241424 |
| Mgi Id | MGI:5902451 | Doi | 10.1371/journal.ppat.1004635 |
| Citation | Lee HM, et al. (2015) IFNgamma signaling endows DCs with the capacity to control type I inflammation during parasitic infection through promoting T-bet+ regulatory T cells. PLoS Pathog 11(2):e1004635 |
| abstractText | IFNgamma signaling drives dendritic cells (DCs) to promote type I T cell (Th1) immunity. Here, we show that activation of DCs by IFNgamma is equally crucial for the differentiation of a population of T-bet+ regulatory T (Treg) cells specialized to inhibit Th1 immune responses. Conditional deletion of IFNgamma receptor in DCs but not in Treg cells resulted in a severe defect in this specific Treg cell subset, leading to exacerbated immune pathology during parasitic infections. Mechanistically, IFNgamma-unresponsive DCs failed to produce sufficient amount of IL-27, a cytokine required for optimal T-bet induction in Treg cells. Thus, IFNgamma signalling endows DCs with the ability to efficiently control a specific type of T cell immunity through promoting a corresponding Treg cell population. |
