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.