Topical Remibrutinib Attenuates LL37-Induced Rosacea-Like Dermatitis by Inhibiting BTK Activation, NF-κB Signaling and Mast Cell Activation

Background

Rosacea is a chronic inflammatory skin disorder in which LL37-driven mast cell activation contributes to cutaneous inflammation. Bruton’s tyrosine kinase (BTK) is a key regulator of canonical IgE-dependent mast cell responses; however, its role in LL37-induced, IgE-independent mast cell activation remains unclear. This study investigated the involvement of BTK activation and nuclear factor-κB (NF-κB) signaling in LL37-induced mast cell activation and evaluated the therapeutic effects of topical remibrutinib in experimental rosacea-like dermatitis.