Skin constitutes a barrier between our body and outside environment providing the first line defence against microbial infection. Epithelial repair and skin wound healing starts with inflammation to clear up invading pathogens and debris followed by cell proliferation and tissue remodelling. The immune response is vital for protecting the body from infection and diseases, however, it remains controversial whether the immune cells contribute to wound closure and tissue repair, or cause scarring and pathology. In this thesis, I investigate the role of Notch signalling in epithelial tissue repair. I demonstrate Notch1 signalling activation in epidermal keratinocytes following acute skin injury recruits innate lymphoid cells (i.e. ILC3s) to the site of injury in a TNF-α/CCL20-dependent mechanism and controls macrophage/monocyte recruitment via ILC3-dependent CCL3. Notch1 also induces epidermal production of IL23 which facilitates ILC3s to produce IL22 for re-epithelialization and skin repair.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:600949 |
| Date | January 2014 |
| Creators | Li, Zhi |
| Publisher | Durham University |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | http://etheses.dur.ac.uk/10524/ |
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