| First Author | Hock H | Year | 2003 |
| Journal | Immunity | Volume | 18 |
| Issue | 1 | Pages | 109-20 |
| PubMed ID | 12530980 | Mgi Jnum | J:81364 |
| Mgi Id | MGI:2449212 | Doi | 10.1016/s1074-7613(02)00501-0 |
| Citation | Hock H, et al. (2003) Intrinsic requirement for zinc finger transcription factor gfi-1 in neutrophil differentiation. Immunity 18(1):109-20 |
| abstractText | We report essential roles of zinc finger transcription factor Gfi-1 in myeloid development. Gene-targeted Gfi-1(-/-) mice lack normal neutrophils and are highly susceptible to abscess formation by gram-positive bacteria. Arrested, morphologically atypical, Gr1(+)Mac1(+) myeloid cells expand with age in the bone marrow. RNAs encoding primary but not secondary or tertiary neutrophil (granulocyte) granule proteins are expressed. The atypical Gr1(+)Mac1(+) cell population shares characteristics of both the neutrophil and macrophage lineages and exhibits phagocytosis and respiratory burst activity. Reexpression of Gfi-1 in sorted Gfi-1(-/-) progenitors ex vivo rescues neutrophil differentiation in response to G-CSF. Thus, Gfi-1 not only promotes differentiation of neutrophils but also antagonizes traits of the alternate monocyte/macrophage program. |
