Abstract
Atopic dermatitis (AD) is a prevalent, persistent inflammatory skin disorder distinguished by pruritic and irritated skin. Toll-like receptors (TLRs) are specialized receptors that recognize specific patterns associated with pathogens and tissue damage, triggering an innate immune response that protects the host from invading pathogens. Previously, it was demonstrated that intradermal injection of the humanized anti-TLR2 monoclonal antibody (Ab) Tomaralimab effectively relieved AD-like skin inflammation in BALB/c mouse models exposed to house dust mite extracts. However, it remains unclear whether allergenic hapten-induced AD can be effectively treated with systemically administered TLR2-targeting Abs. In the present study, it was observed that administrating Tomaralimab through intravenous injection alleviated AD-like skin lesions in BALB/c mice challenged with topical application of 2,4-dinitrochlorobenzene by reducing the infiltration of inflammatory cells into skin lesions and preventing the creation of various inflammatory cytokines, including thymic stromal lymphopoietin, interleukin (IL)-4, IL-13, IL-17 and IL-31, which are associated with the pathogenesis of AD. These findings support the feasibility of using a humanized anti-TLR2 monoclonal Ab as systemic therapy for AD.