The Effect of Anti-CεmX on IgE Production

Atopic Dermatitis

IgE, Atopic Dermatitis, antibody, allergy

Despite the success of Omalizumab that neutralizes free IgE in blood and interstitial fluids, treatment of many allergic disorders remains an unmet medical need. Omalizumab was approved for patients having serum IgE levels in the range of 30-700 IU/ml. Omalizumab may not be effective for patients with much higher serum IgE levels, such as those with atopic dermatitis. Therefore, an alternative approach that targets IgE-committed B cells directly and inhibits the synthesis of IgE without binding to free IgE will be attractive. Anti-CεmX mAb, developed by Dr. TW Chang in Academia Sinica, binds human mIgE+ cells, including IgE-committed lymphoblasts and memory B cells. Such anti-CεmX mAbs should be able to activate B cell receptor (BCR) signaling, which leads to anergy or apoptosis of mIgE+ B lymphoblasts, and induces ADCC through their Fc portion. Depletion of mIgE+ B cells by anti-CεmX treatment would inhibit the formation of IgE-producing plasma cells, resulting in a long-term attenuation of IgE synthesis that would eventually lead to a desensitized state in allergic patients.

This study will collect blood from patients of high serum IgE levels to investigate the function of h4b12, a humanized mAb specific for mIgE+ B cells, and compare the effects of h4B12, Omalizumab, and Rituxumab on the suppression of IgE production and the number of IgE-producing plasma cells. These blood specimens will be collected from 50 patients of atopic dermatitis or urticaria with high serum IgE levels. Fountain Biopharma will carry out the following two in vitro assays to measure the efficacy of h4B12: * IgE ELISA to determine the concentration of IgE. * IgE ELISPOTto determine the number of IgE-producing plasma cells.

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