| First Author | Rathinam C | Year | 2005 |
| Journal | Immunity | Volume | 22 |
| Issue | 6 | Pages | 717-28 |
| PubMed ID | 15963786 | Mgi Jnum | J:99109 |
| Mgi Id | MGI:3581117 | Doi | 10.1016/j.immuni.2005.04.007 |
| Citation | Rathinam C, et al. (2005) The Transcriptional Repressor Gfi1 Controls STAT3-Dependent Dendritic Cell Development and Function. Immunity 22(6):717-28 |
| abstractText | The mechanisms controlling the differentiation of dendritic cells (DCs) remain largely unknown. Using a transcriptional profiling approach, we identified Gfi1 as a novel critical transcription factor in DC differentiation. Gfi1(-/-) mice showed a global reduction of myeloid and lymphoid DCs in all lymphoid organs whereas epidermal Langerhans cells were enhanced in number. In vivo, Gfi1(-/-) DCs showed striking phenotypic and functional alterations such as defective maturation and increased cytokine production. In vitro, Gfi1(-/-) hematopoietic progenitor cells were unable to develop into DCs. Instead, they differentiated into macrophages, suggesting that Gfi1 is a critical modulator of DC versus macrophage development. Analysis of hematopoietic chimeras and retrovirus-reconstituted hematopoietic progenitor cells established a cell autonomous and nonredundant role for Gfi1 in DC development. The developmental defect of Gfi1(-/-) progenitor cells was associated with decreased STAT3 activation. In conclusion, we have identified Gfi1 as a critical transcription factor that controls DC versus macrophage development and dissociates DC maturation and activation. |
