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GATA1-Deficient Dendritic Cells Display Impaired CCL21-Dependent Migration toward Lymph Nodes Due to Reduced Levels of Polysialic Acid.
- Source :
-
Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2016 Dec 01; Vol. 197 (11), pp. 4312-4324. Date of Electronic Publication: 2016 Nov 04. - Publication Year :
- 2016
-
Abstract
- Dendritic cells (DCs) play a pivotal role in the regulation of the immune response. DC development and activation is finely orchestrated through transcriptional programs. GATA1 transcription factor is required for murine DC development, and data suggest that it might be involved in the fine-tuning of the life span and function of activated DCs. We generated DC-specific Gata1 knockout mice (Gata1-KO <superscript>DC</superscript> ), which presented a 20% reduction of splenic DCs, partially explained by enhanced apoptosis. RNA sequencing analysis revealed a number of deregulated genes involved in cell survival, migration, and function. DC migration toward peripheral lymph nodes was impaired in Gata1-KO <superscript>DC</superscript> mice. Migration assays performed in vitro showed that this defect was selective for CCL21, but not CCL19. Interestingly, we show that Gata1-KO <superscript>DC</superscript> DCs have reduced polysialic acid levels on their surface, which is a known determinant for the proper migration of DCs toward CCL21.<br /> (Copyright © 2016 by The American Association of Immunologists, Inc.)
- Subjects :
- Animals
Cell Movement genetics
Chemokine CCL19 genetics
Chemokine CCL19 immunology
Chemokine CCL21 genetics
Dendritic Cells cytology
GATA1 Transcription Factor deficiency
Lymph Nodes cytology
Mice
Mice, Knockout
Sialic Acids genetics
Cell Movement immunology
Chemokine CCL21 immunology
Dendritic Cells immunology
GATA1 Transcription Factor immunology
Lymph Nodes immunology
Sialic Acids immunology
Subjects
Details
- Language :
- English
- ISSN :
- 1550-6606
- Volume :
- 197
- Issue :
- 11
- Database :
- MEDLINE
- Journal :
- Journal of immunology (Baltimore, Md. : 1950)
- Publication Type :
- Academic Journal
- Accession number :
- 27815426
- Full Text :
- https://doi.org/10.4049/jimmunol.1600103