Aiming to IgE: Drug development in allergic diseases

The incidence of allergic disease significantly increases in recent decades, causing it become a major public health problem all over the world. The common allergic diseases such as allergic dermatitis, allergy rhinitis, allergic asthma and food allergy are mediated, at least in part, by immunoglobulin E (IgE), and so IgE acts as a central role in allergic diseases. IgE can interact with its high-affinity receptor (FcεRⅠ) which is primarily expressed on tissue-resident mast cells and circulating basophils, initiating intracellular signal transduction and then causing the activation and degranulation of mast cells and basophils. On the other hand, IgE interaction with its low-affinity receptor (CD23), can regulate various IgE-mediated immune responses including IgE-allergen complex presentation, IgE synthesis, the growth and differentiation of both B and T cells, and the secretion of pro-inflammatory mediators. With the deeper mechanism research for allergic diseases, new therapeutic strategies for interfering IgE are developed and receive a great attention. In this review, we summarize a current profile of therapeutic strategies for interfering IgE in allergic diseases. Besides, we suggest that targeting memory B cells (including long-lived plasma cells and (or) IgE+ memory B cells) may help to completely control allergic diseases, and highlight that the development of drugs synergistically aiming to multiple targets can be a better choice for improving treatment efficacy which results from allergic diseases as the systemic disorders caused by an impaired immune system.