Abstract
Dendritic cells (DC) are the only hematopoietic cells expressing the epithelial specific Ets transcription factor ESE-3. Here we analyzed presence and quantity of isoforms ESE-3a, ESE-3b and ESE-3j in various immunogenic and tolerogenic human monocyte-derived DC (moDC) and blood DC populations using quantitative real time PCR and immunoblot analyses. ESE-3a and ESE-3b were detectable in all moDC populations with ESE-3b being the main transcript. ESE-3b expression was upregulated in immunogenic moDC and downregulated in tolerogenic moDC compared to immature moDC. ESE-3a had similar transcript levels in immature and immunogenic moDC and had very low levels in tolerogenic moDC. In blood DC populations only splice variant ESE-3b was detectable. ESE-3j was not detectable in any of the DC populations. These findings suggest that ESE-3b is the functionally most important ESE-3 isoform in DC.
Highlights
Dendritic cells (DC) are the most potent antigen presenting cells with the unique ability to induce and maintain primary immune responses [1]
We previously reported that the epithelial specific E26 transformation specific (Ets) transcription factor ESE-3 is upregulated in monocyte-derived DC (moDC) stimulated with different compounds whereas IL-10 treatment inhibiting DC development from monocytes impedes induction of ESE-3 expression [15]
It was shown previously that ESE-3 is localized in the nucleus [31], but the antibody used did not discriminate between the different isoforms
Summary
Dendritic cells (DC) are the most potent antigen presenting cells with the unique ability to induce and maintain primary immune responses [1]. DC acquire antigens and migrate to the lymph nodes where peptide antigens are presented to T lymphocytes. During this pathway, immature DC, capable of antigen uptake, differentiate into mature DC. Mature DC are characterized by high surface expression of MHC class II and costimulatory molecules able to induce an immune response. In the absence of maturation stimuli, DC present self-peptide-MHC complexes to circulating naive T cells in peripheral lymphoid organs. In the case of autoreactivity, the T cells will be deleted or become anergic, thereby avoiding autoimmunity [3,4,5]
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