Atopic dermatitis (AD) is a chronic inflammatory skin disease with T cell activation as a key feature, in which TH2 cell–mediated responses play a pivotal role. Regulatory T cells (Tregs) are central immune cells restricting autoimmunity and autoinflammation in our body. Patients with immune dysregulation, polyendocrinopathy, and enteropathy X-linked syndrome (IPEX), an immune disease with a deficiency in CD25+ Tregs, characteristically develop skin inflammation and allergic disorders. Foxp3 mutant mice spontaneously exhibit allergic airway inflammation, AD–like skin disease, and increased serum IgE levels. Which indicates that Tregs play a crucial role in the development of allergic skin inflammation. We investigated the underlying mechanisms by which Tregs control cutaneous allergic inflammation. The depletion of Foxp3+ Tregs led to significantly exacerbated AD-like skin inflammation, including increased recruitment of neutrophils and expression of Th2 cytokines, such as IL-5,13, IFN-γ. Neutrophils were one of the major inflammatory cell types infiltrated in Treg-depleted AD-like mouse skin. Neutrophil infiltrating in skin of Treg-depleted mice released more neutrophil extracellular traps (NETs) than wild type. NETosis is a unique cell death pathway of neutrophils. During NETosis, neutrophils produce and release NETs. IFN-γ gene expression was highly enhanced in Treg-depleted AD-like lesional skin, which triggered neutrophilic infiltration and the formation of NETs. Neutralization of IFN-γ abolished neutrophil infiltration and NETosis in Treg-depleted mice. Neutrophils stimulated with IFN-γ were more prone to release NETs in vitro. Finally, Foxp3+ Treg control cutaneous allergic inflammation by regulating IFN-γ-driven neutrophilic infiltration and NETosis. Our results highlight the previously underestimated Treg-IFN-γ-neutrophil inflammatory axis, which may provide new therapeutic strategies for the treatment of allergic dermatitis.