Premium
Activation of Peroxisome Proliferator‐activated Receptor Gamma Leads to Upregulation of ESE ‐3 Expression in Human Monocyte‐derived Dendritic Cells
Author(s) -
Sprater F.,
Azeem W.,
Appel S.
Publication year - 2014
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12126
Subject(s) - downregulation and upregulation , peroxisome proliferator activated receptor , microbiology and biotechnology , monocyte , dendritic cell , receptor , immunogenicity , chemistry , transcription factor , biology , immunology , immune system , gene , biochemistry
The transcription factor ESE ‐3 has been suggested to be involved in regulating the immunogenicity of human monocyte‐derived dendritic cells (mo DC s). While ESE ‐3 is not expressed in monocytes, it is upregulated during the differentiation of monocytes into dendritic cells ( DC s) and highly expressed in immunogenic DC s while downregulated in tolerogenic DC s. Activation of peroxisome proliferator‐activated receptor gamma ( PPAR ‐ γ ) during DC development has been shown to result in a rather tolerogenic cell population. In this study, we identified eight PPAR ‐ γ binding sites upstream of the ESE ‐3 gene. Activation of the PPAR ‐ γ pathway with synthetic PPAR ‐ γ ligands during mo DC generation resulted in upregulation of ESE ‐3b expression on mRNA and protein level, phenotypic alterations and reduced capacity of the cells to stimulate allogeneic T cells. This could be inhibited by blocking the PPAR ‐ γ pathway with specific antagonists. Our results suggest PPAR ‐ γ to be involved in the regulation of ESE ‐3b expression during mo DC development and that ESE ‐3 expression is not correlated with the immunogenicity of DC s.