New molecules in management of atopic dermatitis

Atopic dermatitis (AD) is a complex inflammatory dermatosis that is heterogeneous in terms of clinical manifestations and molecular profiles. The current immunopathogenic model of AD is focused on the activation of type 2 immune cells, including Th2 cells, innate lymphoid cells 2, eosinophils, mast cells, and basophils, with varying degrees of involvement from other pathways such as Th22, Th1, and Th17. The massive amount of research carried out in the past decade to comprehend the molecular basis of AD has allowed the development of new targeted drugs. In addition to revolutionary treatments for severe AD, such as the Interleukin (IL)-4Ra inhibitor dupilumab, the anti-IL-13 inhibitor tralokinumab, the anti-IL-31 inhibitor nemolizumab, and the Janus Kinase (JAK) inhibitors, more than 50 new medications are currently under development. While all ethnic groups exhibit Th2 and Th22 hyperactivation, the East Asian endotype of AD is additionally distinguished by an elevated Th17-mediated signal, while African Americans do not exhibit Th1/Th17 skewing. The ethnic heterogeneity of AD may hold important therapeutic implications, as a patient’s genetic predisposition may influence treatment response, and, thereby, a tailored strategy that better targets the dominant immunologic pathways in each ethnic subgroup may be envisioned.