Biomarker prediction of pediatric atopic dermatitis severity

Autor: Mark H Kaplan, Sarah Engle, Ching-Yun Chang, Allyson Satterwhite, Benjamin Ulrich, Tristan Hayes, Robert Tepper, Jonathan Sims
Rok vydání: 2020
Předmět:
Zdroj: The Journal of Immunology. 204:147.20-147.20
ISSN: 1550-6606
0022-1767
DOI: 10.4049/jimmunol.204.supp.147.20
Popis: Atopic dermatitis (AD) is a chronic inflammatory skin disease that affects 25% of children and 1–3% of adults worldwide, and has increased 2- to 3-fold over the past several decades. The pathogenesis of AD may result from complex interactions between environmental and genetic factors, barrier defects and immune dysregulation resulting in epidermal hyperplasia and increased penetration of allergens and microbial pathogens. Although most cases of AD are transient, and AD is often thought of as the first step of the atopic march, some AD patients have active disease throughout life. In this study, we analyzed a population of infants that were at high risk for atopic disease and sampled serum, analyzed peripheral blood mononuclear cells, and clinical parameters upon entry (mean age 10.3 months) and five years later. We tested 161 serum analytes using a combination of single-plex, multiplex, Olink, and Quanterix assays. Broadly, the concentration of many analytes fell over time, while SDF and sCD40L concentration increased at the later time point. Several analytes correlated with AD severity as assessed by SCORAD, and most significantly, IL-13 and MCP-4 correlated with SCORAD at both time points. Subsets of cytokines were significantly correlated with each other, consistent with early disease skewing toward type 2 immune response, and two subsets were correlated with percentages of NKT cells or Th2 cells in the peripheral blood. Importantly, forward selection modeling identified 33 infant serum analytes that could be used to predict AD severity five years later (r2=0.85, p=0.042). This dataset will likely have predictive value for AD persistence past infancy and will be useful in further defining the pathogenesis of atopic disease.
Databáze: OpenAIRE