Dendritic cell populations in patients with self-reported food hypersensitivity

Abstract

Self-reported hypersensitivity to food is a common condition and many of these patients have indications of intestinal immune activation. Dendritic cells (DCs) are recognized as the most potent antigen-presenting cells involved in both initiating immune responses and maintaining tolerance. The aims of this study were to evaluate the DC populations with their phenotype and T cell stimulatory capacity in patients with food hypersensitivity and to study its relationship with atopic disease. Blood samples from 10 patients with self-reported food hypersensitivity, divided into atopic and nonatopic subgroups, and 10 gender- and age-matched healthy controls were analyzed by flow cytometry using the Miltenyi Blood Dendritic cells kit. Monocyte-derived DCs (moDCs) were evaluated concerning their phenotype and T cell stimulatory capacity. DC populations and cell surface markers were not significantly different between patients and healthy controls, but moDCs from atopic patients expressed significantly more CD38 compared to moDCs from nonatopic patients. Moreover, lipopolysaccharide stimulated moDCs from atopic patients produced significantly more interleukin-10 compared to nonatopic patients. CD38 expression was correlated to total serum immunoglobulin E levels. These findings support the notion of immune activation in some patients with self-reported food hypersensitivity. They need to be confirmed in a larger cohort.

Keywords:

• food hypersensitivity
• atopy
• dendritic cells
• CD38

Acknowledgments/Disclosure

We thank all patients and healthy controls for kindly donating blood for our study and Dagny Ann Sandnes and Marie Karlsen for excellent technical help. The authors have been financially supported by the Faculty of Medicine and Dentistry at the University of Bergen, the Strategic Research Program at Helse Bergen, the Western Norway Health Authority, the Broegelmann Foundation, the Norwegian Cancer Society and Bergen Research Foundation. The authors report no conflicts of interest in this work.