Type 2 inflammation is driven by the adaptive and innate immune systems. It plays a central role in defending against pathogens by activating type 2 helper cells (TH2) and type 2 innate lymphoid cells (ILC2), which drive inflammation through the production of type 2 cytokines such as interleukin (IL)-4 and IL-13. While type 2 inflammation is an essential weapon in protecting against pathogens, its dysregulation can lead to chronic damage of the epithelium. Dysregulated type 2 inflammation manifests as a variety of common epithelial diseases, such as atopic dermatitis (AD), allergic asthma (AA) and eosinophilic esophagitis. The observed correlation of AD and AA led to the hypothesis of the "atopic march", which refers to the progression from AD in infants to AA in children and adults, with both conditions caused by type 2 inflammation. Recent studies suggest that this progression may result from an inter-epithelial crosstalk between the skin and the lungs. The cytokine thymic stromal lymphopoietin (TSLP), a known driver of type 2 inflammation, has been identified as a major contributor to the atopic march. TSLP is an IL-7-like cytokine involved in the activation and maturation of dendritic cells as well as the direct activation of CD4 + T cells.