Atopic Dermatitis: Immune Endotypes and the OX40-OX40L Pathway

Author: Sanofi Editorial Team

Sanofi Editorial Team

Introduction

Atopic dermatitis (AD) is a common, chronic inflammatory skin disease that typically begins early in life (1). AD follows a relapsing–remitting course, and persistence of symptoms into adulthood contributes to its chronic nature, with up to 50% of affected children showing disease in later life (1). Globally, AD affects 20% of children and 10% of adults, with increasing incidence in industrialized countries (1). Loss of epithelial barrier integrity facilitates disease progression (1). During chronic inflammation, tumour necrosis factor receptor superfamily member 4; TNFRSF4 (OX40)-expressing T helper cells (Th1, Th17, and Th22) cells are recruited, and sustained OX40– OX40 ligand (OX40L) signalling promotes their proliferation (2). The resulting cytokines (IFN-γ, IL-17, IL-22) drive keratinocyte proliferation, epidermal thickening, and further immune cell recruitment, contributing to chronic AD (2).

Abbreviations:

AD – Atopic dermatitis; APC – Antigen-presenting cell; IgE – Immunoglobulin E; OX40 – Tumor necrosis factor receptor superfamily member 4 (CD134); OX40L – OX40 ligand (CD252); T cell – T lymphocyte; CD4⁺ – Cluster of differentiation 4 positive; Th – T helper cell; Th1 – Type 1 T helper cell; Th2 – Type 2 T helper cell; Th9 – Type 9 T helper cell; Th17 – Type 17 T helper cell; Th22 – Type 22 T helper cell; Treg – Regulatory T cell; IFN-γ – Interferon gamma; IL – Interleukin

References

MAT-SA-2600198-V1-APRIL2026

Introduction

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