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

Abstract：

: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.

journal_name

Immunity

journal_title

Immunity

authors

Hock H,Hamblen MJ,Rooke HM,Traver D,Bronson RT,Cameron S,Orkin SH

doi

10.1016/s1074-7613(02)00501-0

keywords:

subject

Has Abstract

pub_date

2003-01-01 00:00:00

pages

109-20

issue

1

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(02)00501-0

journal_volume

18

pub_type

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