P38 MAPK Signaling Mediates Retinoic Acid-Induced CD103 Expression in Human Dendritic Cells.

In this study, we analyzed the cell type specificity and the molecular mechanisms involved in RA-induced CD103 expression. We show that RA treatment caused a significant upregulation of CD103 in differentiated monocyte-derived DCs and blood DCs, but not in differentiated monocyte-derived macrophages or T cells. DC treatment with an RARα agonist lead to a similar increase in CD103 expression as RA treatment, while RARA gene silencing with siRNA blocked RA-induced upregulation of CD103, pointing to a major role of RARα in the regulation of CD103 expression. To elucidate RA-induced signaling downstream of RARα, we used Western blot analysis of RA-treated DCs and showed a significant increase of p38 MAPK phosphorylation. In addition, DCs cultured with RA and a p38 MAPK inhibitor had a significantly reduced expression of CD103 compared with DCs cultured with RA only, indicating that p38 MAPK is involved in CD103 regulation. In summary, these findings suggest that the RA-induced expression of CD103 is specific to DCs, is mediated primarily through RARα and involves p38 MAPK signaling. PMID: 32737889 [PubMed - as supplied by publisher]
Source: Immunology - Category: Allergy & Immunology Authors: Tags: Immunology Source Type: research