Lay summary
Atopic dermatitis (AD) is a chronic allergic skin condition affecting a significant proportion of New Zealand’s population. It is characterised by skin infiltration of a type of immune cell (CD4+ T cell) that expresses chemical messengers called IL-13. Specialised non-circulating CD4+ T cells, termed tissue resident memory cells (TRMs), persist in peripheral tissues to provide rapid protection against repeated infection. Human studies show that IL-13+ TRMs in AD are resistant to treatment and persist in the skin after inflammation has cleared, contributing to recurring skin flare-up. This research will use gene editing technology and mouse models of AD to identify the key genes and signals needed for these cells to form and survive in the skin. By understanding these mechanisms, we aim to uncover new therapeutic targets to impair TRM survival and improve quality of life for those affected by this persistent and distressing condition.