Langerhans Cell Modulation in Atopic Dermatitis Is TLR2/SOCS1-Dependent and JAK Inhibitor-Sensitive.

ABSTRACT:

Background

Langerhans cells (LC) are epidermal dendritic cells building the skin's outermost immunological barrier and bridging innate and adaptive immune responses. Their sensing property of the microbiome via Toll-like receptors (TLR) is impaired in atopic dermatitis (AD). We hypothesize a desensitization of LC because of persistent Staphylococcus aureus exposure in AD and underlying mechanisms being TLR2-related.

Methods

Human LC generated from hematopoetic stem cells were desensitized via repetitive exposure to TLR2-ligands (priming) and compared to unprimed cells for their TLR-responsiveness. JAK inhibitors impact was evaluated. Maturation marker, migration marker and behavior, cytokine release, and downstream molecule regulation were addressed by flow cytometry, qPCR,

SUBMITTER: Deng Y 

PROVIDER: S-EPMC12444830 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature