Cause of Atopic Itching Identified... 3D Artificial Skin Model Mimicking Patient Skin Developed

Enabling prediction of individual drug responses
"Applicable to new drug evaluation and prediction of treatment responses"

Korean researchers have developed a three-dimensional artificial skin model that reproduces the lesion microenvironment of patients with atopic dermatitis. It is expected to be used as a platform for predicting patient-specific drug responses, supporting new drug evaluation and the establishment of personalized treatment strategies.

Korean researchers recreated the lesion microenvironment of atopic dermatitis patients. Yonsei University College of Medicine.

The research team led by Professor Kim Rakyun of the Department of Biomedical Science at Yonsei University College of Medicine announced on the 19th that, through joint research with the teams of Professors Park Kyungmin and Choi Jungmin at Incheon National University, they have built a three-dimensional artificial skin model that mimics the inflammation and hypoxic environment of atopic dermatitis in a way that closely resembles real skin.

Previous studies relied on two-dimensional cell cultures or animal models, which could not sufficiently capture the interactions among structural cells, immune cells, and sensory neurons observed in actual patient skin. In particular, itching, the core symptom of atopic dermatitis, is a phenomenon in which structural cells, immune responses, and the nervous system are intricately intertwined beyond simple inflammatory reactions, but experimental platforms capable of comprehensively analyzing these interactions have been limited.

The research team first used single-cell RNA sequencing analysis to identify a "COL6A5-positive fibroblast subtype" that overexpresses itch-inducing factors. This cell type was found to interact with sensory nerves and showed the potential to be involved in the induction of chronic itching.

The team then used a gelatin-based hydrogel to fabricate a three-dimensional construct in which these cells can survive. By precisely controlling oxygen diffusion, they recreated the hypoxic conditions observed in lesions, and by applying immune-stimulating factors, they reproduced an inflammatory microenvironment.

In experiments, cells exposed to hypoxic conditions showed increased expression of itch-related factors, and real-time activation of co-cultured sensory neurons was observed. This experimentally demonstrated that itching in atopic dermatitis arises from interactions among skin structural cells, the immune system, and the nervous system.

The researchers explained that they designed the experimental model based on large-scale patient genomic data, thereby narrowing the gap between clinical settings and laboratory conditions. Because it can reflect human disease characteristics while reducing dependence on animal testing, it is expected to be highly useful for evaluating the efficacy of new drug candidates and for precision medicine research.

Professor Kim, who led the study, said, "This will serve as a technological foundation that can be applied to establishing patient-tailored treatment strategies," adding, "We plan to extend this research beyond atopic dermatitis to various chronic inflammatory skin diseases." The study results were recently published in the international journal Bioactive Materials.

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