Intravenous immunoglobulin-mediated regulation of Notch ligands on human dendritic cells

摘要

To the Editor:Massoud et al demonstrated that intravenous immunoglobulin (IVIg) attenuates airway inflammation through induction of FoxP3~+ regulatory T (Treg) cells.They found that IVIg-primed dendritic cells (DCs) in ovalbumin-exposed mice exhibited decreased Jagged-1 and increased Delta-4 expression. Thus, the authors conclude that reduced T_H2 responses and induction of Treg cells by IVIg might involve modulation of Notch ligands on CD11c~+ lung DCs. As IVIg is also beneficial in patients involving predominant T_H1 responses, we explored whether data from mouse DCs under T_H2 pathologies could be translated to human DCs activated under T_H1promoting conditions. We studied the expression of not only Jagged-1 and Delta-4 but also all Notch ligands. Monocyte-derived DCs were stimulated with TLR4-agonist LPS for 24 hours. The effect of equimolar concentrations (0.15 mmol/L) of IVIg or irrelevant protein control human serum albumin on the expression of all the Notch ligands was analyzed (see this article's Online Repository at www.jacionline.org).