https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14649 Sat 24 Mar 2018 08:20:54 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11486 Sat 24 Mar 2018 08:10:26 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17772 Sat 24 Mar 2018 07:57:40 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:5109 Sat 24 Mar 2018 07:48:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:5180 Sat 24 Mar 2018 07:47:49 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24090 Aspergillus fumigatus allergen mouse model of EoE. Because IL-33 induction was transient in this model and chronicity of IL-33 expression has been demonstrated in humans, naive mice were treated with recombinant IL-33 for 1 wk and esophageal pathology was evaluated. IL-33 application produced changes consistent with phenotypically early EoE, including transmural eosinophilia, mucosal hyperproliferation, and upregulation of eosinophilic genes and chemokines. Th2 cytokines, including IL-13, along with innate lymphoid cell group 2, Th1/17, and M2 macrophage marker genes, were increased after IL-33 application. IL-33-induced eosinophilia was ablated in IL-13 null mice. In addition, IL-33 induced a profound inhibition of the regulatory T cell gene signature. We conclude that IL-33 gene expression is associated with pediatric EoE development and that application of recombinant protein in mice phenocopies the early clinical phase of the human disease in an IL-13-dependent manner. IL-33 inhibition of esophageal regulatory T cell function may induce loss of antigenic tolerance, thereby providing a mechanistic rationale for EoE development.]]> Fri 03 Dec 2021 10:32:37 AEDT ]]>