IL-33-activated dendritic cells are critical for allergic airway inflammation.
Eur J Immunol
; 41(6): 1675-86, 2011 Jun.
Article
en En
| MEDLINE
| ID: mdl-21469105
ABSTRACT
IL-33, a new member of the IL-1 family cytokine, is involved in Th2-type responses in a wide range of diseases and signals through the ST2 receptor expressed on many immune cells. Since the effects of IL-33 on DCs remain controversial, we investigated the ability of IL-33 to modulate DC functions in vitro and in vivo. Here, we report that IL-33 activates myeloid DCs to produce IL-6, IL-1b, TNF, CCL17 and to express high levels of CD40, CD80 OX40L and CCR7. Importantly, IL-33-activated DCs prime naive lymphocytes to produce the Th2 cytokines IL-5 and IL-13, but not IL-4. In vivo, IL-33 exposure induces DC recruitment and activation in the lung. Using an OVA-induced allergic lung inflammation model, we demonstrate that the reduced airway inflammation in ST2-deficient mice correlates with the failure in DC activation and migration to the draining LN. Finally, we show that adoptive transfer of IL-33-activated DCs exacerbates lung inflammation in a DC-driven model of allergic airway inflammation. These data demonstrate for the first time that IL-33 activates DCs during antigen presentation and thereby drives a Th2-type response in allergic lung inflammation.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Hipersensibilidad Respiratoria
/
Células Dendríticas
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Citocinas
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Interleucinas
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Receptores de Interleucina
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Células Th2
Límite:
Animals
Idioma:
En
Revista:
Eur J Immunol
Año:
2011
Tipo del documento:
Article
País de afiliación:
Francia