IL-33-activated dendritic cells are critical for allergic airway inflammation

被引:259
作者
Besnard, Anne-Gaelle [1 ,2 ]
Togbe, Dieudonnee [1 ,2 ,3 ]
Guillou, Noelline [1 ,2 ]
Erard, Francois [1 ,2 ]
Quesniaux, Valerie [1 ,2 ]
Ryffel, Bernhard [1 ,2 ]
机构
[1] Univ Orleans, F-45071 Orleans 2, France
[2] CNRS, UMR 6218, F-45071 Orleans, France
[3] Artimmune SAS, Ctr Innovat, Orleans, France
关键词
Allergy; Cytokines; DC; IL-33; Lung inflammation; HUMAN BASOPHILS; MURINE MODEL; IL-33; RECEPTOR; CYTOKINE; EXPRESSION; T1/ST2; TYPE-2; PROTEIN; MEMBER;
D O I
10.1002/eji.201041033
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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-1 beta, 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.
引用
收藏
页码:1675 / 1686
页数:12
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