K. Reich et al., Engagement of the Fc epsilon RI stimulates the production of IL-16 in Langerhans cell-like dendritic cells, J IMMUNOL, 167(11), 2001, pp. 6321-6329
Preferential uptake and presentation of IgE-bound allergens by epidermal La
ngerhans cells (LC) via the high affinity IgE receptor, Fe epsilon RI, is r
egarded as an important mechanism in the induction of cutaneous inflammatio
n in atopic dermatitis. Here, we show that activation of monocyte-derived L
C-like dendritic cells (LLDC) through engagement of Fc epsilon RI induces t
he expression of IL-16, a chemoattractant factor for dendritic cells, CD4() T cells, and eosinophils. We found that ligation of Fc epsilon RI on LLDC
derived from atopic dermatitis patients that express high levels of FC eps
ilon RI increases IL-16 mRNA expression and storage of intracellular IL-16
protein and enhances the secretion of mature IL-16 in a biphasic manner. An
early release of IL-16 (peak at 4 h) is independent of protein synthesis,
while a more delayed release (peak at 12 h) requires protein synthesis and
occurs subsequent to the induction of IL-16 mRNA and intracellular accumula
tion of pro-IL-16. There was evidence that LLDC use caspase-1 to process IL
-16, as inhibition of caspase-1, but not of caspase-3, partially prevented
the release of IL-16 in response to ligation of Fc epsilon RI. In an in viv
o model of IgE-dependent LC activation, the atopy patch test, positive skin
reactions were also associated with the induction of IL-16 in epidermal de
ndritic cells. These data indicate that IL-16 released from LC. after aller
gen-mediated activation through Fc epsilon RI may link IgE-driven and cellu
lar inflammatory responses in diseases such as atopic dermatitis.