Retinoic acid-induced upregulation of αE integrin (CD103) is TGFβ-dependent in human dendritic cells

• Published in: The Journal of immunology (1950) 2016-05, Vol.196 (1_Supplement), p.59-59.19
• Main Authors: Roe, Mandi M, Swain, Steven D, Bimczok, Diane
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.196.Supp.59.19

CD103 (αE integrin) is thought to mediate the cross-talk between dendritic and epithelial cells. Based on a recent study showing retinoic acid (RA) may enhance CD103 expression at high concentrations (Hartog, Allergy and Immunology. 2013), we examined monocyte-derived dendritic cell (MoDC) CD103 expression levels with physiological concentrations of RA (100nM) under serum-free conditions. FACS analysis revealed that RA induced a significant increase of MoDCs positive for both extracellular and intracellular CD103 expression. Gene expression analysis corroborated these results with a 57-fold increase in ITGAE upon RA culture. Moreover, expression of β7, which forms the αEβ7 integrin heterodimer with CD103, was similarly upregulated by RA. We next evaluated the TGFβ-dependence of RA-induced CD103 regulation based on a study showing that itgαE gene expression in mice is regulated by TGFβ in T-cells (Robinson, Immunology. 2001). MoDCs were cultured with RA and SB431542, a TGFβR inhibitor that blocks SMAD phosphorylation. When MoDCs were cultured with RA and SB431542, CD103 expression was significantly reduced when compared to MoDCs cultured with RA alone (p