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Characterization of hematopoietic GATA transcription factor expression in mouse and human dendritic cells.

Authors :
Scheenstra MR
Salunkhe V
De Cuyper IM
Hoogenboezem M
Li E
Kuijpers TW
van den Berg TK
GutiƩrrez L
Source :
Blood cells, molecules & diseases [Blood Cells Mol Dis] 2015 Dec; Vol. 55 (4), pp. 293-303. Date of Electronic Publication: 2015 Jul 14.
Publication Year :
2015

Abstract

Dendritic cells (DCs) are key initiators and regulators of the immune response. The development of the DC lineage and their subsets requires an orchestrated regulation of their transcriptional program. Gata1, a transcription factor expressed in several hematopoietic cell lineages, has been recently reported to be required for mouse DC development and function. In humans, GATA1 is involved in the lineage separation between monocyte-derived DCs and Langerhans cells (LC) and loss of GATA1 results in differentiation arrest at the monocyte stage. The hematopoietic GATA factors (i.e. Gata1, Gata2, Gata3) are known to regulate each other's expression and to function consecutively throughout lineage commitment (so-called GATA switch). In humans, mutations in GATA2 are causative of MonoMAC disease, a human immunodeficiency syndrome characterized by loss of DCs, monocytes, B and NK cells. However, additional data on the expression of hematopoietic GATA factors in the DC lineage is missing. In this study, we have characterized the expression of hematopoietic GATA factors in murine and human DCs and their expression dynamics upon TLR stimulation. We found that all hematopoietic GATA factors are expressed in DCs, but identified species-specific differences in the relative expression of each GATA factor, and how their expression fluctuates upon stimulation.<br /> (Copyright © 2015 Elsevier Inc. All rights reserved.)

Details

Language :
English
ISSN :
1096-0961
Volume :
55
Issue :
4
Database :
MEDLINE
Journal :
Blood cells, molecules & diseases
Publication Type :
Academic Journal
Accession number :
26460250
Full Text :
https://doi.org/10.1016/j.bcmd.2015.07.006