Therapeutic strategies for eosinophilic dermatoses.

• The management of eosinophilic dermatoses should consider the underlying pathomechanism. • Causes of eosinophilia are either intrinsic (in eosinophils), or extrinsic (via cytokines). • Antibodies against IL-5 or its receptor target eosinophil numbers and activation. • Dexpramipexole efficiently reduces eosinophil numbers. • Tyrosine kinase inhibitors are effective in FIP1L1-PDGFRA positive hypereosinophilia. Eosinophil infiltration is observed in a broad spectrum of skin diseases of various origins. Eosinophils are thought to actively contribute to pathogenesis as they are able to defend against microbes, to regulate inflammation, cause tissue damage, promote remodeling and fibrosis, and initiate pruritus. Therefore, targeting eosinophils would seem a worthwhile therapeutic approach. A promising strategy is to target the production, activation and survival of eosinophils, example with antibodies directed against IL-5 or its receptor, and Siglec-8. Dexpramipexole and tyrosine kinase inhibitors have been shown to reduce eosinophil numbers in patients with hypereosinophilia. Janus kinase inhibitors block signal transduction and thus activation of inflammatory cells including eosinophils. A further approach is to target cells and cytokines acting on or mediators released by eosinophils, for example, CD52, IL-13, IL-31, TSLP, and eotaxins. This review summarizes current therapeutic strategies, including novel agents affecting eosinophils directly that are under clinical investigation. [ABSTRACT FROM AUTHOR]