The type 2 cytokine IL-4 promotes atopic dermatitis but also the resolution of inflammation. The function of IL-4 during the resolution of atopic inflammation is poorly known. In a model of calcipotriol induced atopic dermatitis, we show that basophils are systemically activated by TSLP to produce IL-4. Basophils are the main source of IL-4 in the skin in this model, and directed the proliferation and differentiation of keratinocytes to promote an epidermal dysfunction. However, at the same time, basophils derived IL-4 and M-CSF inhibited the accumulation of proinflammatory leucocytes in the skin while promoting the expansion and function of M2-like pro-resolution macrophages. Thus basophils and IL-4 can play both beneficial and detrimental roles at the same time during atopic skin inflammation.