Intrinsic requirement for zinc finger transcription factor Gfi-1 in neutrophil differentiation.

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B-Lymphocytes, Bacterial-Infections, Bone-Marrow-Cells, Cell-Differentiation, DNA-Binding-Proteins, Growth-Disorders, Macrophages, Mice, Mice-Knockout, Models-Biological, Neutrophils, Phagocytosis, Phenotype, Respiratory-Burst, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S, T-Lymphocytes, Transcription-Factors, Zinc-Fingers

JAX Source

Immunity 2003 Jan; 18(1):109-20.


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.