https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:11837 Wed 11 Apr 2018 16:30:22 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14146 Wed 11 Apr 2018 15:12:12 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15241 + T cells. We found that a limited number of microRNAs exhibited marked up- or downregulation following early-life infection and sensitisation, for many of which the levels of expression were further changed following chronic challenge with the sensitizing antigen. Targets of these microRNAs included genes involved in immune or inflammatory responses (e.g. Gata3, Kitl) and in tissue remodelling (e.g. Igf1, Tgfbr1), as well as genes for various transcription factors and signalling proteins. In pulmonary CD4⁺ T cells, there was significant demethylation at promoter sites for interleukin-4 and interferon-γ, the latter increasing following chronic challenge. We conclude that, in this model, progression to an asthmatic phenotype is linked to epigenetic regulation of genes associated with inflammation and structural remodelling, and with T-cell commitment to a Th2 immunological response. Epigenetic changes associated with this pattern of gene activation might play a role in the development of childhood asthma.]]> Wed 11 Apr 2018 14:44:33 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10124 Wed 11 Apr 2018 10:19:59 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:11339 Sat 24 Mar 2018 08:08:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:5638 Sat 24 Mar 2018 07:44:01 AEDT ]]>