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* ZAUM-Center for Allergy and Environment, Division of Environmental Dermatology and Allergy, GSF National Research Center for Environment and Health/Technische Universität München, Munich, Germany;
Department of Dermatology and Allergy Biederstein, Technische Universität München, Munich, Germany;
Allergy Research Group, University Medical Center, Freiburg, Germany; and
Julius-von-Sachs-Institute of Biosciences, Division of Pharmaceutical Biology, University of Würzburg, Würzburg, Germany
The immune response of atopic individuals against allergens is characterized by increased levels of Th2 cytokines and chemokines. However, the way in which the cytokine/chemokine profile is matched to the type of invading allergen, and why these profiles sometimes derail and lead to disease, is not well understood. We recently demonstrated that pollen modulates dendritic cell (DC) function in a way that results in an enhanced capacity to initiate Th2 responses in vitro. Here, we examined the effects of aqueous birch pollen extracts (Bet.-APE) on chemokine receptor expression and chemokine production by human monocyte-derived DCs. Bet.-APE strongly induced expression and function of CXCR4 and reduced CCR1 and CCR5 expression on immature DCs. In addition, DC treatment with Bet.-APE significantly reduced LPS-induced production of CXCL10/IP-10, CCL5/RANTES; induced CCL22/macrophage-derived chemokine; and did not significantly change release of CCL17/thymus and activation-regulated chemokine. At a functional level, Bet.-APE increased the capacity of LPS-stimulated DCs to attract Th2 cells, whereas the capacity to recruit Th1 cells was reduced. Bet.-APE significantly and dose-dependently enhanced intracellular cAMP, suggesting that water-soluble factors from pollen grains bind a G
s-protein-coupled receptor. E1-Phytoprostanes were identified to be one player in the Th2-polarizing potential of aqueous pollen extracts. In summary, our results demonstrate that pollen itself releases regulatory mediators which generate a Th2-promoting micromilieu with preferential recruitment of Th2 cells to the site of pollen exposure.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 The study was supported by a Bundesministerium für Bildung, Wissenschaft, Forschung und Technologie Grant (to T.J. and C.T.-H.), V.M. was supported by a research fellowship from the Bayerische Forschungsstiftung, and C.T.-H. was a recipient of the Bayerische Habilitationsförderpreis.
2 Address correspondence and reprint requests to Dr. Claudia Traidl-Hoffmann, Division of Environmental Dermatology and Allergy, GSF National Research Center for Environment and Health/Technische Universität München, ZAUM-Center for Allergy and Environment, Technische Universität Munich, Biedersteinerstrasse 29, Munich, Germany. E-mail address: Claudia.traidl-hoffmann{at}lrz.tum.de
3 Abbreviations used in this paper: DC, dendritic cell; TARC, thymus and activation-regulated chemokine; MDC, macrophage-derived chemokine; MoDC, monocyte-derived DC; PPE1, pollen-associated phytoprostane; Bet.-APE, Betula alba L. aqueous pollen extract.
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