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Engagement of the FcRI Stimulates the Production of IL-16 in Langerhans Cell-Like Dendritic Cells^{1 ,2}

Kristian Reich^3,*, Andrea Heine^*, Sabine Hugo^*, Volker Blaschke^*, Peter Middel, Arthur Kaser, Herbert Tilg, Sabine Blaschke, Carsten Gutgesell^* and Christine Neumann^*

Departments of ^* Dermatology, Pathology, and Rheumatology/Nephrology, Georg- August-University, Göttingen, Germany; and Division of Gastroenterology and Hepatology, Department of Medicine, University Hospital Innsbruck, Innsbruck, Austria

Preferential uptake and presentation of IgE-bound allergens by epidermal Langerhans cells (LC) via the high affinity IgE receptor, FcRI, is regarded as an important mechanism in the induction of cutaneous inflammation in atopic dermatitis. Here, we show that activation of monocyte-derived LC-like dendritic cells (LLDC) through engagement of FcRI induces the expression of IL-16, a chemoattractant factor for dendritic cells, CD4⁺ T cells, and eosinophils. We found that ligation of FcRI on LLDC derived from atopic dermatitis patients that express high levels of FcRI 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 accumulation 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 FcRI. In an in vivo model of IgE-dependent LC activation, the atopy patch test, positive skin reactions were also associated with the induction of IL-16 in epidermal dendritic cells. These data indicate that IL-16 released from LC after allergen-mediated activation through FcRI may link IgE-driven and cellular inflammatory responses in diseases such as atopic dermatitis.

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