The influence of skin microbial ecology on γδ T-cell immune pathways in allergic dermatitis models in mice.

Abstract

Atopic dermatitis is a complex disease influenced by alterations in the skin microbiome and immune dysregulation. Despite the recognized role of these factors, the specific pathways by which distinct microbial populations affect skin immunity remain insufficiently understood. On a molecular level, the pathogenesis of atopic dermatitis involves critical cytokines such as IL-4, IL-17, interferon-γ, and IL-10, which contribute to the imbalance in T helper cell responses. Importantly, gamma-delta (γδ) T cells, which produce these cytokines and infiltrate affected epithelial cells in atopic dermatitis, have been underexplored. This study seeks to alleviate atopic dermatitis symptoms in mice by adjusting both peripheral and local immune environments through the transplantation of skin microbiota. By employing 16S rRNA sequencing, we characterized the skin microbiome of the mouse model. Our results demonstrate that microbiota intervention significantly reduces skin thickening and serum IgE levels in DNCB-induced atopic dermatitis mice. Additionally, changes in skin microbiota modulated immune cell dynamics, restoring the T helper 1 / T helper 2 balance and leading to clinical improvement. These findings highlight the critical role of skin microbiota in shaping immune responses, positioning microbiota-based therapies as a potential treatment for atopic dermatitis.