| First Author | Feuerer M | Year | 2006 |
| Journal | J Immunol | Volume | 176 |
| Issue | 5 | Pages | 2857-63 |
| PubMed ID | 16493042 | Mgi Jnum | J:129422 |
| Mgi Id | MGI:3769227 | Doi | 10.4049/jimmunol.176.5.2857 |
| Citation | Feuerer M, et al. (2006) Self-limitation of Th1-mediated inflammation by IFN-gamma. J Immunol 176(5):2857-63 |
| abstractText | IFN-gamma is an effector cytokine of cell-mediated immunity that plays an essential role in both innate and adaptive phases of an immune response. Interestingly, in several Th1-dependent autoimmune models, lack of IFN-gamma is associated with an acceleration of disease. To distinguish the influence of IFN-gamma on the polarization of naive precursors from the influence on effector cells, we used an adoptive transfer model of differentiated Ag-specific Th1 cells. In this study, IFN-gamma displayed a dual function in a Th1-dependent immune reaction. In the early phase, IFN-gamma accelerated the inflammation, whereas in the late phase it mediated the process of self-limitation. We demonstrated that IFN-gamma limits the number of Th1 effector cells after Ag challenge. Studies using IFN-gammaR-/- mice as recipients showed that IFN-gamma acts indirectly via host cells to regulate the pool size of Th1 cells. NO was a downstream effector molecule. Transfer experiments of Th1 cells into IFN-gamma-/- mice revealed that Th1 cells control both themselves and the corresponding inflammation by the release of IFN-gamma. Thus, the proinflammatory cytokine IFN-gamma can act as a negative feedback regulator to control Th1-mediated immune responses. |
