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Comparative analysis of candidate gene expression in Asian atopic dermatitis and psoriasis: identification of shared
Hye Li Kim1,2, Dong Eun Kim3, KeLun Zhang1,2
1Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea.
Background:
Atopic dermatitis (AD) and psoriasis are chronic inflammatory skin diseases with distinct molecular profiles, but their clinical differentiation in Asian patients is often difficult due to overlapping or atypical features. This study aimed to identify differentially expressed genes (DEGs) and pathways in lesional skin to explore potential diagnostic and therapeutic targets.
Methods:
To identify molecular differences, we performed transcriptomic analysis of lesional skin from patients with AD, psoriasis, and healthy controls (HCs). DEGs were identified by comparing each disease group with HCs, and selected targets were validated using immunofluorescence staining.
Results:
Filaggrin (FLG) expression was significantly decreased in both the AD (p = 0.0043) and psoriasis (p = 0.0012) compared to HCs. Moreover, loricrin (LOR) expression was significantly reduced in both the AD (p = 0.0043) and psoriasis (p = 0.0082) relative to HCs. Serine protease inhibitor Kazal-type 5 (SPINK5) expression was markedly elevated in the psoriasis (p = 0.0012), but was significantly decreased in AD (p = 0.0173). Additionally, serpin family B member 4 (SERPINB4) expression was significantly upregulated in both AD (p = 0.0043) and psoriasis (p = 0.0012) relative to HCs. Immunofluorescence analysis of human skin samples confirmed these transcriptomic findings at the protein level.
Conclusion:
FLG, LOR, and SERPINB4 showed shared expression alterations in AD and psoriasis, whereas SPINK5 demonstrated the most consistent differential expression pattern between the two diseases. These findings suggest that SPINK5 may represent a candidate molecular signature for distinguishing AD from psoriasis, and provide insight into shared and distinct molecular mechanisms underlying these diseases in Asian patients.
