Olink

Olink®
Part of Thermo Fisher Scientific

Proteomic characterization of atopic dermatitis blood from infancy to adulthood

Journal of the American Academy of Dermatology, 2023

Del Duca E., Renert-Yuval Y., Pavel A., Mikhaylov D., Wu J., Lefferdink R., Fang M., Sheth A., Blumstein A., Facheris P., Estrada Y., Rangel S., Krueger J., Paller A., Guttman-Yassky E.

Disease areaApplication areaSample typeProducts
Dermatological Diseases
Patient Stratification
Serum
Olink Target 96

Olink Target 96

Abstract

Background: Atopic dermatitis/AD patients have systemic biomarker dysregulation that differs by age group, but proteomic characteristics of these age-based changes are unknown.

Objective: To profile blood proteins of AD patients across different age groups versus age-appropriate controls.

Methods: Using the OLINK high-throughput proteomic platform, we profiled 375 serum proteins of 20 infants (0-5y/o), 39 children (6-11y/o), 21 adolescents (12-17y/o), and 20 adults (≥18y/o) with moderate-to-severe AD, and 83 age-appropriate controls.

Results: Each group presented a distinct systemic proteomic signature. Th2-related proteins were increased in infant AD and further intensified with age through adolescence and adulthood (IL-4/CCL13/CCL17). In contrast, Th1 axis down-regulation was detected in infants with AD and gradually reversed to increased Th1 products (IFNγ/CXCL9/CXCL10/CCL2) in AD patients from childhood to adulthood. Despite their short disease duration, infants already have evidence of systemic inflammation, with significant up-regulation of innate immunity (IL-17C/IL-1RN), T-cell activation/migration (CCL19), Th2 (CCL13/CCL17), and Th17 (PI3) proteins. AD Adults present unique up-regulation of cardiovascular proteins related with coagulation and diabetes.

Limitations: Cross-sectional observational study with a single time-point.

Conclusions: Systemic immune signatures of AD are age-specific beyond the shared Th2 immune activation. These data advocate for precision medicine approaches based on age-specific AD profiles.

Read publication ↗