Comprehensive molecular profiling of Hispanic, Black, Asian, and White atopic dermatitis via tape strip RNAseq and serum proteomics
Journal of Allergy and Clinical Immunology, 2026
Liu D., Del Duca E., Brunner P., Avallone G., Beaziz J., Metukuru R., Lin X., Estrada Y., Lau M., Largen J., Ungar B., Guttman-Yassky E.
| Disease area | Application area | Sample type | Products |
|---|---|---|---|
Immunological & Inflammatory Diseases Dermatological Diseases | Patient Stratification | Serum |  Olink Target 96 |
Abstract
Background
Atopic dermatitis (AD) is a heterogeneous inflammatory skin disease with known ethnic disparities in clinical presentation and treatment response. However, molecular data, particularly for Hispanic patients, remain limited.
Objective
To characterize the molecular phenotype of AD across Hispanic, Black, Asian, and White patients using tape strip transcriptomic and blood proteomic profiling.
Methods
We enrolled 47 AD patients (9 Hispanic, 14 Black, 11 Asian, 13 White) and 40 controls. Tape strips and serum were collected for RNA sequencing and proteomic analysis, respectively. Differential expression, pathway enrichment, and gene-clinical correlations were analyzed across ethnicities.
Results
Across ethnicities, we identified shared immune activation in lesional and nonlesional AD skin, including upregulation of Th1-related (e.g., IL12B, TNF), Th2-related (e.g., CCL17, IL13), and Th17-related (e.g., CXCL1/2, IL6) pathways. However, gene-level drivers varied: Th1-related markers (e.g., CXCL10) were more elevated in White and Black patients; Th17 axis skewing was most pronounced in Asian patients; and Th22 and JAK3 signaling showed greater activation in White and Black patients. Hispanic patients demonstrated a mixed immune phenotype resembling both White and Black AD. Barrier dysfunction, including filaggrin deficiency and lipid synthesis defects, was universal, with Asian patients exhibiting the most pronounced lipid-related gene downregulation. Proteomic data mirrored transcriptomic trends and highlighted broad systemic inflammation in Hispanic patients. White patients exhibited the strongest correlations between lesional gene expression and disease severity, though differences in clinical presentation and global scoring methods may influence these correlations across skin tones.
Conclusion
This multi-omic, multi-ethnic analysis reveals both shared and ethnicity-specific molecular signatures in AD, with the first in-depth profiling of Hispanic patients. These findings may inform future precision-targeted therapies across diverse populations.