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

Eva Sallmann; Bärbel Reininger; Sabine Brandt; Nikolaus Duschek; Elisabeth Hoflehner; Erika Garner-Spitzer; Barbara Platzer; Eleonora Dehlink; Martina Hammer; Martin Holcmann; Hans C Oettgen; Ursula Wiedermann; Maria Sibilia; Edda Fiebiger; Antal Rot; Dieter Maurer

doi:10.4049/jimmunol.1003392

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

Eva Sallmann, Bärbel Reininger, Sabine Brandt, Nikolaus Duschek, Elisabeth Hoflehner, Erika Garner-Spitzer, Barbara Platzer, Eleonora Dehlink, Martina Hammer, Martin Holcmann, Hans C Oettgen, Ursula Wiedermann, Maria Sibilia, Edda Fiebiger, Antal Rot, Dieter Maurer

Research output: Contribution to journal › Article › peer-review

Abstract

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.

Original language	English
Pages (from-to)	164-71
Number of pages	8
Journal	Journal of Immunology
Volume	187
Issue number	1
Early online date	27 May 2011
DOIs	https://doi.org/10.4049/jimmunol.1003392
Publication status	Published - 1 Jul 2011

Keywords

Allergens
Animals
Antigens, Plant
Cells, Cultured
Coculture Techniques
Dendritic Cells
Female
Humans
Inflammation Mediators
Male
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Ovalbumin
Protein Binding
Receptors, IgE
Th2 Cells
Time Factors

Access to Document

10.4049/jimmunol.1003392

Cite this

Sallmann, E., Reininger, B., Brandt, S., Duschek, N., Hoflehner, E., Garner-Spitzer, E., Platzer, B., Dehlink, E., Hammer, M., Holcmann, M., Oettgen, H. C., Wiedermann, U., Sibilia, M., Fiebiger, E., Rot, A., & Maurer, D. (2011). High-affinity IgE receptors on dendritic cells exacerbate Th2-dependent inflammation. Journal of Immunology, 187(1), 164-71. https://doi.org/10.4049/jimmunol.1003392

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title = "High-affinity IgE receptors on dendritic cells exacerbate Th2-dependent inflammation",

abstract = "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.",

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author = "Eva Sallmann and B{\"a}rbel Reininger and Sabine Brandt and Nikolaus Duschek and Elisabeth Hoflehner and Erika Garner-Spitzer and Barbara Platzer and Eleonora Dehlink and Martina Hammer and Martin Holcmann and Oettgen, {Hans C} and Ursula Wiedermann and Maria Sibilia and Edda Fiebiger and Antal Rot and Dieter Maurer",

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doi = "10.4049/jimmunol.1003392",

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Sallmann, E, Reininger, B, Brandt, S, Duschek, N, Hoflehner, E, Garner-Spitzer, E, Platzer, B, Dehlink, E, Hammer, M, Holcmann, M, Oettgen, HC, Wiedermann, U, Sibilia, M, Fiebiger, E, Rot, A & Maurer, D 2011, 'High-affinity IgE receptors on dendritic cells exacerbate Th2-dependent inflammation', Journal of Immunology, vol. 187, no. 1, pp. 164-71. https://doi.org/10.4049/jimmunol.1003392

TY - JOUR

T1 - High-affinity IgE receptors on dendritic cells exacerbate Th2-dependent inflammation

AU - Sallmann, Eva

AU - Reininger, Bärbel

AU - Brandt, Sabine

AU - Duschek, Nikolaus

AU - Hoflehner, Elisabeth

AU - Garner-Spitzer, Erika

AU - Platzer, Barbara

AU - Dehlink, Eleonora

AU - Hammer, Martina

AU - Holcmann, Martin

AU - Oettgen, Hans C

AU - Wiedermann, Ursula

AU - Sibilia, Maria

AU - Fiebiger, Edda

AU - Rot, Antal

AU - Maurer, Dieter

PY - 2011/7/1

Y1 - 2011/7/1

N2 - 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.

AB - 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.

KW - Allergens

KW - Animals

KW - Antigens, Plant

KW - Cells, Cultured

KW - Coculture Techniques

KW - Dendritic Cells

KW - Female

KW - Humans

KW - Inflammation Mediators

KW - Male

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Ovalbumin

KW - Protein Binding

KW - Receptors, IgE

KW - Th2 Cells

KW - Time Factors

U2 - 10.4049/jimmunol.1003392

DO - 10.4049/jimmunol.1003392

M3 - Article

C2 - 21622859

SN - 0022-1767

VL - 187

SP - 164

EP - 171

JO - Journal of Immunology

JF - Journal of Immunology

IS - 1

ER -