Abstract
Dupilumab, a human monoclonal antibody that binds to IL-4Ra and inhibits IL-4 and IL-13 signaling, improves inflammation and itch in patients with atopic dermatitis (AD). IL-4 signals through the type I (IL-4Ra and IL-2Rg) and type II receptors (IL-4Ra and IL-13Ra1), while IL-13 signaling is restricted to the type II receptor. By binding to shared receptor chain, IL-4Ra, dupilumab prevents the action of both cytokines. To deconstruct the individual roles of IL-4 and IL-13 in the context of AD, we evaluated receptor expression and cytokine-dependent effects in relevant cell types implicated in disease pathobiology.
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