Targeting immunoglobulin E in atopic dermatitis: A review of the existing evidence

Abstract

Immunoglobulin E (IgE) plays an essential role in many allergic diseases. This review highlights the role of IgE in atopic dermatitis (AD), a common, chronic, and complex skin inflammation, and the available therapeutic approaches that target IgE in AD. We examine the existing data showing the use of omalizumab, the only biologic anti-IgE therapy available in clinical use, plasma apheresis, and a combination of both therapeutic approaches for the treatment of AD. Existing data on the efficacy of omalizumab in AD are inconclusive. A limited number of randomised controlled studies, few uncontrolled prospective and retrospective reports, as well as multiple case series and case reports observed varying degrees of the efficacy of omalizumab in AD. Omalizumab displays a trend of higher efficacy in AD patients with low IgE levels compared with those with very high-to-extremely high serum IgE concentrations. Plasma apheresis and its combination with omalizumab show good efficacy, even in patients with unusually high serum IgE concentrations. Combining apheresis and anti-IgE treatment may serve as a comprehensive therapeutic approach for patients with elevated levels of IgE. Dedicated clinical studies with robust study designs are needed to establish the therapeutic efficacy of omalizumab in AD.

Keywords: Apheresis; Atopic dermatitis; Biologics; Immunoglobulin E; Omalizumab.

Fig. 1

Simplified mechanism of AD and the role of IgE. Antigen penetration through damaged skin and presentation via APCs leads to a Th2 response. The resulting IgE production against the antigen can lead to degranulation of mast cells in the presence of the external antigen or food allergens causing a local inflammatory response and recruitment of other inflammatory cells such as EoS. LCs and IDCs activated via recognizing pathogen-derived antigens, promote Th1 and Th2 driven immune responses in acute AD lesions. Omalizumab, by neutralizing IgE, can inhibit mast cell degranulation and dendritic cell activation. AD, atopic dermatitis; EoS, eosinophils; IDC, inflammatory dendritic cells; IgE, immunoglobulin E; IL, interleukin; LC, Langerhans cells; Th2, T helper cell.

Fig. 2

Patient population, their baseline IgE levels, and corresponding clinical outcome of treatment of AD with omalizumab in terms of percentage change from baseline in SCORAD/DLQI/Pruritus/EASI scores in various studies. Size of the dots are proportional to the number of patients analysed. Hotze et al., 2013 showing deterioration consists of all patients with FLG mutations DLQI, dermatological life quality index; EASI, Eczema Area and Severity Index; FLG, filaggrin gene; IgE, immunoglobulin E; SCORAD, scoring atopic dermatitis.