Atopic dermatitis (AD) is a prevalent and complex chronic inflammatory skin condition that typically emerges in early childhood but can affect individuals at any age. Although more than 50% of affected children experience spontaneous remission, growing evidence suggests AD as a lifelong condition characterized by heterogeneous disease trajectories, variable clinical expression, and a persistent risk of relapse. Despite significant advances in understanding AD pathogenesis, the mechanisms governing remission, recurrence, and persistence remain poorly understood, and long-term studies that comprehensively characterize the full spectrum of disease trajectories are still lacking.

We aim to define the cellular and molecular landscapes that shape the course of atopic dermatitis from disease onset and flares to remission and relapse. A central question driving our work is how inflammatory memory is encoded and distributed across circulating and tissue-resident immune cells as well as stromal cells, and how this memory governs long-term disease behavior.

We characterize AD-specific molecular changes across different phases of disease activity and integrate comprehensive registry data on lifestyle, environmental exposures, and related factors to identify the key determinants that influence disease course. By characterizing the molecular mechanisms, specific cell subtypes, and cellular communities that sustain remission or trigger relapse, we aim to generate insights that directly inform the development of new therapies particularly those targeting epigenetic regulatory mechanisms as well as prevention strategies centered on modifiable environmental factors.