The pathogenesis of atopic dermatitis (AD) is multifactorial and complex. Consequently, clinical signs and symptoms vary strongly depending on individually relevant trigger factors and the stage of the disease. So far, treatment of AD was commonly limited to topical treatment or, in more severe cases, to systemic drugs mostly approved for other indications than AD. However, emerging data on new anti-inflammatory agents have been published in the recent years. As these new substances specifically focus on immune responses in AD, these are partially considered as possible 'breakthrough' in the treatment of AD. Therapeutic strategies of the future appear to be 'customized' for inflammation in AD as they target pro-inflammatory, highly relevant cytokines and cytokine receptors, such as IL-4Rα, IL-13, IL-31, and IL-17. Further innovative therapeutic approaches aim to block the function of relevant molecules such as thymic stromal lymphopoietin, chemoattractant-receptor homologous molecule expressed on Th2 lymphocytes (CRTh2), and phosphodiesterase (PDE)-4 inhibitors. Recently, anti-inflammatory effects in AD by antagonizing the histamine (H)-4 receptor have also been detected. Finally, specific immunotherapy is under further investigation as treatment option for AD patients with clinically relevant sensitization.
Keywords: atopic dermatitis; interleukin; molecule; receptor; treatment.
© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.