Content » Vol 100, March

Investigative Report

The OX40 Axis is Associated with Both Systemic and Local Involvement in Atopic Dermatitis

Julie Sophie Hohwü Elsner, Michael Carlsson, Julie Kristine Stougaard, Uffe Nygaard, Matthias Buchner, Regina Fölster-Holst, Malene Hvid, Christian Vestergaard, Mette Deleuran, Bent Deleuran
DOI: 10.2340/00015555-3452

Abstract

Atopic dermatitis (AD) is a chronic, or chronically relapsing, inflammatory skin disease associated with asthma and allergic rhinitis, and is dominated by Th2 cells. The co-stimulatory T-cell receptor OX40 and its ligand, OX40L, play a central role in the pathogenesis of AD, as their interactions are crucial for the generation of TH2 memory cells. Using enzyme-linked immunoassay (ELISA) and flow cytometry on blood samples from patients with AD and healthy volunteers, this study shows that the serum level of soluble (s) OX40 is decreased in patients with AD, and the expression of OX40 by activated skin-homing CD4+ T cells is increased. This study further shows, using immunofluorescence on skin biopsies, that OX40+ and OX40L+ cells are co-located within the dermis, indicating local activity of OX40/OX40L. Serum levels of sOX40 were associated with atopic diseases and, together, these results support that the OX40 system is important for chronic inflammation in AD skin.

Significance

Atopic dermatitis is a chronic, or chronically relapsing, inflammatory skin disease dominated by Th2 cells. The co-stimulatory T-cell receptor OX40 and its ligand, OX40L, are crucial for the generation of Th2 memory cells, and may thus play a central role in the pathogenesis and chronicity of atopic dermatitis. This study shows that OX40 expression is increased on skin-homing T cells in patients with atopic dermatitis, and that OX40 and OX40L cells are co-localized in the skin. These findings indicate that the OX40 system could play a pivotal role in the inflammatory reaction of atopic dermatitis in the skin.

Supplementary content

Comments

Not logged in! You need to login/create an account to comment on articles. Click here to login/create an account.