High-affinity IgE receptors on dendritic cells exacerbate Th2-dependent inflammation

The IgE-mediated and Th2-dependent late-phase reaction remains a mechanistically enigmatic and daunting element of human allergic inflammation. In this study, we uncover the FcεRI on dendritic cells (DCs) as a key in vivo component of this form of allergy. Because rodent, unlike human, DCs lack FcεR...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2011-07, Vol.187 (1), p.164-171
Main Authors: Sallmann, Eva, Reininger, Bärbel, Brandt, Sabine, Duschek, Nikolaus, Hoflehner, Elisabeth, Garner-Spitzer, Erika, Platzer, Barbara, Dehlink, Eleonora, Hammer, Martina, Holcmann, Martin, Oettgen, Hans C, Wiedermann, Ursula, Sibilia, Maria, Fiebiger, Edda, Rot, Antal, Maurer, Dieter
Format: Article
Language:English
Subjects:
Allergens - toxicity
Animals
Antigens, Plant - toxicity
Cells, Cultured
Coculture Techniques
Dendritic Cells - immunology
Dendritic Cells - metabolism
Dendritic Cells - pathology
Female
Humans
Inflammation Mediators - metabolism
Inflammation Mediators - physiology
Inflammation Mediators - toxicity
Male
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Ovalbumin - toxicity
Protein Binding - genetics
Protein Binding - immunology
Receptors, IgE - deficiency
Receptors, IgE - metabolism
Receptors, IgE - physiology
Th2 Cells - immunology
Th2 Cells - metabolism
Th2 Cells - pathology
Time Factors
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Summary:The IgE-mediated and Th2-dependent late-phase reaction remains a mechanistically enigmatic and daunting element of human allergic inflammation. In this study, we uncover the FcεRI on dendritic cells (DCs) as a key in vivo component of this form of allergy. Because rodent, unlike human, DCs lack FcεRI, this mechanism could be revealed only by using a new transgenic mouse model with human-like FcεRI expression on DCs. In the presence of IgE and allergen, FcεRI(+) DCs instructed naive T cells to differentiate into Th2 cells in vitro and boosted allergen-specific Th2 responses and Th2-dependent eosinophilia at the site of allergen exposure in vivo. Thus, FcεRI on DCs drives the cascade of pathogenic reactions linking the initial allergen capture by IgE with subsequent Th2-dominated T cell responses and the development of late-phase allergic tissue inflammation.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.1003392