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The Major Birch Pollen Allergen Bet v 1 Induces Different Responses in…

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PLoS One. 2015 Jan 30;10(1):e0117904. doi: 10.1371/journal.pone.0117904. eCollection 2015.

The Major Birch Pollen Allergen Bet v 1 Induces Different Responses in Dendritic Cells of Birch Pollen Allergic and Healthy Individuals.

Smole U1, Radauer C2, Lengger N2, Svoboda M2, Rigby N3, Bublin M2, Gaier S2, Hoffmann-Sommergruber K2, Jensen-Jarolim E4, Mechtcheriakova D2, Breiteneder H2.

Author information

  • 1Department of Pathophysiology and Allergy Research; Center for Pathophysiology, Infectiology, and Immunology, Medical University of Vienna, Vienna, Austria; Department of Environmental Health Sciences, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, United States of America.
  • 2Department of Pathophysiology and Allergy Research; Center for Pathophysiology, Infectiology, and Immunology, Medical University of Vienna, Vienna, Austria.
  • 3Institute of Food Research, Norwich Research Park, Norwich, United Kingdom.
  • 4Department of Pathophysiology and Allergy Research; Center for Pathophysiology, Infectiology, and Immunology, Medical University of Vienna, Vienna, Austria; Messerli Research Institute of the Medical University of Vienna, Veterinary University of Vienna and University of Vienna, Austria.

Abstract

Dendritic cells play a fundamental role in shaping the immune response to allergens. The events that lead to allergic sensitization or tolerance induction during the interaction of the major birch pollen allergen Bet v 1 and dendritic cells are not very well studied. Here, we analyzed the uptake of Bet v 1 and the cross-reactive celery allergen Api g 1 by immature monocyte-derived dendritic cells (iMoDCs) of allergic and normal donors. In addition, we characterized the allergen-triggered intracellular signaling and transcriptional events. Uptake kinetics, competitive binding, and internalization pathways of labeled allergens by iMoDCs were visualized by live-cell imaging. Surface-bound IgE was detected by immunofluorescence microscopy and flow cytometry. Allergen- and IgE-induced gene expression of early growth response genes and Th1 and Th2 related cytokines and chemokines were analyzed by real-time PCR. Phosporylation of signaling kinases was analyzed by Western blot. Internalization of Bet v 1 by iMoDCs of both donor groups, likely by receptor-mediated caveolar endocytosis, followed similar kinetics. Bet v 1 outcompeted Api g 1 in cell surface binding and uptake. MoDCs of allergic and healthy donors displayed surface-bound IgE and showed a pronounced upregulation of Th2 cytokine- and NFκB-dependent genes upon non-specific Fcε receptor cross-linking. In contrast to these IgE-mediated responses, Bet v 1-stimulation increased transcript levels of the Th2 cytokines IL-4 and IL-13 but not of NFκB-related genes in MoDCs of BP allergic donors. Cells of healthy donors were either unresponsive or showed elevated mRNA levels of Th1-promoting chemokines. Moreover, Bet v 1 was able to induce Erk1/2 and p38 MAPK activation in BP allergics but only a slight p38 activation in normal donors. In conclusion, our data indicate that Bet v 1 favors the activation of a Th2 program only in DCs of BP allergic individuals.
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