| First Author | Besnard AG | Year | 2011 |
| Journal | Eur J Immunol | Volume | 41 |
| Issue | 6 | Pages | 1675-86 |
| PubMed ID | 21469105 | Mgi Jnum | J:176634 |
| Mgi Id | MGI:5292322 | Doi | 10.1002/eji.201041033 |
| Citation | Besnard AG, et al. (2011) IL-33-activated dendritic cells are critical for allergic airway inflammation. Eur J Immunol 41(6):1675-86 |
| abstractText | 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. |
