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| Content Provider | PubMed Central |
|---|---|
| Author | Lugo-villarino, Geanncarlo Roberto, Maldonado-lópez Richard, Possemato Peñaranda, Cristina Glimcher, Laurie H. |
| Copyright Year | 2003 |
| Abstract | IFN-γ is well known as the signature cytokine of CD4+ T helper 1, CD8+, and natural killer cells, but recent studies demonstrate that antigen-presenting cells, in particular dendritic cells (DCs), are another potent source for this proinflammatory cytokine. T-bet, a transcription factor that controls IFN-γ expression in CD4+ T cells, was reported recently to be expressed in human monocytes and myeloid DCs. In this study we investigate the role of T-bet in this important cell type. The development, differentiation, and activation of bone marrow and splenic DCs were unimpaired in mice lacking T-bet. However, T-bet was essential for the optimal production of IFN-γ by both CD8α+ and CD8α- DCs. T-bet-deficient DCs were significantly impaired in their capacity to secrete IFN-γ after both stimulation with IL-12 alone or in combination with IL-18. Further, T-bet-/- DCs were impaired in their ability to activate the T helper 1 program of adoptively transferred antigen-specific T cells in vivo. The rapid up-regulation of T-bet by IFN-γ in DCs coupled with a function for DC-derived IFN-γ in T cell activation may constitute a positive feedback loop to maximize type 1 immunity. |
| Related Links | http://dx.doi.org/10.1073/pnas.1332767100 |
| Ending Page | 7754 |
| Page Count | 6 |
| Starting Page | 7749 |
| File Format | |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 13 |
| Volume Number | 100 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2003-06-24 |
| Access Restriction | Open |
| Rights Holder | National Academy of Sciences |
| Subject Keyword | General Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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