Apoptosis on the other hand may inactivate IL-33. It is likely that both inactivation and release of IL-33 take place linking between apoptosis and cell damage in many chronic inflammatory diseases in which GSK-3 inhibitor IL-33 has been detected. The crucial role of IL-33 in asthma has been assumed due to several pieces of evidence. Administration of IL-33 results in lymphocyte-independent airway hyperreactivity, goblet

cell hyperplasia and eosinophilic and monocytic infiltration. Hypertrophy and enhanced mucous secretion in the bronchi and bronchioles occurs after repeated applications in mice 5. In addition, IL-13-dependent differentiation of alveolar macrophages towards alternatively activated macrophages with increased airway inflammation has been reported in a murine model 19. Furthermore,

CD34pos progenitor cells express the receptor for IL-33, ST2, and secrete large amounts of Th2-type cytokines and chemokines in the presence of IL-33. IL-13- and IL-5-expressing CD34pos cells have been found in the sputum of asthmatic individuals and were up-regulated upon allergen-challenge 12. Moreover, IL-33 contributes to the recruitment and activation of eosinophils to the same degree as IL-5. The in vivo relevance of IL-33 in human asthma is further supported by its higher expression in epithelial cells and smooth muscle cells in moderate to severe asthmatics, but not mild asthmatics. This has been confirmed Dabrafenib ic50 at the protein level in broncheoalveolar lavage fluid 20. Finally, a genome-wide association study has reported the association between single nucleotide polymorphisms in the IL-33 gene and in the ST2 gene and an increased risk to develop asthma 21. In conclusion, IL-33 is evolving as a candidate molecule that acts on DCs and bridges innate and adaptive immune responses in the lung. IL-33 thereby affects both the development of allergic sensitization and the aggravation of lung inflammation. The study by Besnard et al. 13 demonstrates this in an elegant way, defining DCs as effector cells in vivo and confirming ST2-specific GNA12 DC activation. However, further work is required to fully delineate the role of IL-33 in allergic disease. Conflict of

interest: The authors declare no financial or commercial conflict of interest. See accompanying article: http://dx.doi.org/10.1002/eji.201041033 “
“In this study, we investigated the characteristics of the infection and subsequent immunity induced by Strongyloides venezuelensis in Lewis rats. Animals were infected with 4000 L3 of S. venezuelensis and number of eggs per gram of faeces indicated an acute phase around day 8 and a recovery phase around day 32 after infection. A strong Th2 polarization during recovery phase was ascertained by a significant increase in IgG1 and IgE compared with that in the acute period. A shift in the cytokine profile confirmed these findings. A predominant production of IFN-γ during the acute phase was followed by IL-10 production during recovery.