Review suggests chemokine inhibition as prospective therapeutic target for atopic dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin disease that commonly causes eczema accompanied by severe itching on pathological skin lesions. Although the pathological mechanisms are not fully understood, epidermal barrier dysfunction and immune dysfunction are critical for the development of AD. Notably, skin-infiltrating immune cells play a crucial role in the development of atopic skin inflammation. Recent studies have demonstrated that the infiltration of inflammatory cells into skin lesion is regulated by various chemokine ligands-receptors interactions. In this review, we focused on the pathogenic role of chemokines and chemokine receptors in AD development. The lesional skin tissues of patients with AD highly express various chemokines to enhance the migration of immune cells via chemokine ligand-receptor interactions. Since thier the inhibition and blockade contribute to the regulation of inflammatory response in the lesional skins of AD, chemokine ligands and/or receptors are prospective targets for AD therapy. In fact, some blocking agents and antagonist have shown positive results in the improvement of the inflammatory phenotypes in AD model mice. Clinical trials are progressing slowly but steadily, suggesting that chemokine ligands-receptors interactions remain a prospective therapeutic target for AD.