Document Detail


The transcription factor Fli-1 regulates monocyte, macrophage and dendritic cell development in mice.
MedLine Citation:
PMID:  23320737     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fli-1 belongs to the Ets transcription factor family and is expressed in haematopoietic cells, including most of the cells that are active in immunity. The mononuclear phagocytes, i.e. monocytes, macrophages and dendritic cells, originate in haematopoietic stem cells and play an important role in immunity. To assess the role of Fli-1 in mononuclear phagocyte development in vivo, we generated mice that express a truncated Fli-1 protein, lacking the C-terminal transcriptional activation domain (Fli-1(Δ) (CTA) ). Fli-1(Δ) (CTA) (/Δ) (CTA) mice had significantly increased populations of haematopoietic stem cells and common dendritic cell precursors in bone marrow compared with wild-type littermates. Significantly increased classical dendritic cells, plasmacytoid dendritic cells, and macrophage populations were found in spleens from Fli-1(∆) (CTA) (/∆) (CTA) mice compared with wild-type littermates. Fli-1(Δ) (CTA) (/Δ) (CTA) mice also had increased pre-classical dendritic cell and monocyte populations in peripheral blood mononuclear cells. Furthermore, bone marrow reconstitution studies demonstrated that expression of Fli-1 in both haematopoietic cells and stromal cells affected mononuclear phagocyte development in mice. Expression of Fms-like tyrosine kinase 3 ligand (Flt3L), a haematopoietic growth factor, in multipotent progenitors was statistically significantly increased from Fli-1(∆) (CTA) (/∆) (CTA) mice compared with wild-type littermates. Fli-1 protein binds directly to the promoter region of the Flt3L gene. Hence, Fli-1 plays an important role in the mononuclear phagocyte development, and the C-terminal transcriptional activation domain of Fli-1 negatively modulates mononuclear phagocyte development.
Authors:
Eiji Suzuki; Sarah Williams; Shuzo Sato; Gary Gilkeson; Dennis K Watson; Xian K Zhang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Immunology     Volume:  139     ISSN:  1365-2567     ISO Abbreviation:  Immunology     Publication Date:  2013 Jul 
Date Detail:
Created Date:  2013-06-14     Completed Date:  2013-08-19     Revised Date:  2014-07-01    
Medline Journal Info:
Nlm Unique ID:  0374672     Medline TA:  Immunology     Country:  England    
Other Details:
Languages:  eng     Pagination:  318-27     Citation Subset:  IM    
Copyright Information:
Published 2013. This article is a U.S. Government work and is in the public domain in the USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bone Marrow / immunology
Cell Differentiation*
Cell Line
Cells, Cultured
Dendritic Cells / cytology*,  immunology
Female
Macrophages / cytology*,  immunology
Male
Membrane Proteins / genetics,  metabolism
Mice
Mice, Inbred C57BL
Monocytes / cytology*,  immunology
Proto-Oncogene Protein c-fli-1 / chemistry,  genetics,  metabolism*
Spleen / immunology
fms-Like Tyrosine Kinase 3 / metabolism*
Grant Support
ID/Acronym/Agency:
AR056670/AR/NIAMS NIH HHS; R01 AR056670/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/Membrane Proteins; 0/Proto-Oncogene Protein c-fli-1; 0/flt3 ligand protein; EC 2.7.10.1/fms-Like Tyrosine Kinase 3
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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