Abstract

Atopic dermatitis is an inflammatory, itchy skin condition characterised by a fluctuating and chronic disease course. Effective therapies inhibit downstream immune signalling of interleukin (IL)-4, IL-13, IL-31,1 and Janus kinase activity.2 Biologics that target upstream cytokines, such as IL-1α, IL-33, and thymic stromal lymphopoietin (TSLP), have so far been unsuccessful. OX40, a cell-surface glycoprotein, which is highly expressed on T cells and dendritic cells in lesional atopic dermatitis skin, works downstream of TSLP; OX40 stimulates proliferation and survival of activated T cells, some of which might become memory T cells.

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