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Patients with atopic dermatitis (AD) have skin barrier dysfunction, which is closely related to keratinocyte (KC) abnormalities. Upon stimulation by external factors, KCs release a large number of inflammatory mediators, thereby activating type 2 inflammation, which, in turn, exacerbates skin barrier dysfunction. Thus, the interaction between KCs and type 2 inflammation is a key factor in the pathogenesis of AD, and exacerbation of inflammation and pruritus. At present, the innovative medications, such as biologics and small molecule drugs, have been shown anti-inflammatory effects in AD. Studies also demonstrate their role in skin barrier repair. Therefore, research on the interaction between KCs and type 2 inflammation will help understand the pathogenesis of AD and provide evidence to optimize treatment strategies for AD.