<P> Regulation of IgE levels through control of B cell differentiation to antibody - secreting plasma cells is thought to involve the "low - affinity" receptor FcεRII, or CD23 . CD23 may also allow facilitated antigen presentation, an IgE - dependent mechanism whereby B cells expressing CD23 are able to present allergen to (and stimulate) specific T helper cells, causing the perpetuation of a Th2 response, one of the hallmarks of which is the production of more antibodies . </P> <P> Diagnosis of allergy is most often done by reviewing a person's medical history and finding a positive result for the presence of allergen specific IgE when conducting a skin or blood test . Specific IgE testing is the proven test for allergy detection; evidence does not show that indiscriminate IgE testing or testing for immunoglobulin G (IgG) can support allergy diagnosis . </P> <P> Currently, allergic diseases and asthma are usually treated with one or more of the following drugs: (1) antihistamines and antileukotrienes, which antagonize the inflammatory mediators histamine and leukotrienes, (2) local or systemic (oral or injectable) corticosteroids, which suppress a broad spectrum of inflammatory mechanisms, (3) short or long - acting bronchodilators, which relax smooth muscle of constricted airway in asthma, or (4) mast cell stabilizers, which inhibit the degranulation of mast cells that is normally triggered by IgE - binding at FcεRI . Long - term uses of systemic corticosteroids are known to cause many serious side effects and are advisable to avoid, if alternative therapies are available . </P> <P> IgE, the IgE synthesis pathway, and the IgE - mediated allergic / inflammatory pathway are all important targets in intervening with the pathological processes of allergy, asthma, and other IgE - mediated diseases . The B lymphocyte differentiation and maturation pathway that eventually generate IgE - secreting plasma cells go through the intermediate steps of IgE - expressing B lymphoblasts and involves the interaction with IgE - expressing memory B cells . Tanox, a biotech company based in Houston, Texas, proposed in 1987 that by targeting membrane - bound IgE (mIgE) on B lymphoblast and memory B cells, those cells can be lysed or down - regulated, thus achieving the inhibition of the production of antigen - specific IgE and hence a shift of immune balance toward non-IgE mechanisms . Two approaches targeting the IgE pathway were evolved and both are in active development . In the first approach, the anti-IgE antibody drug omalizumab (trade name Xolair) recognises IgE not bound to its receptors and is used to neutralise or mop - up existing IgE and prevent it from binding to the receptors on mast cells and basophils . Xolair has been approved in many countries for treating severe, persistent allergic asthma . It has also been approved in March 2014 in the European Union and the U.S. for treating chronic spontaneous urticaria, which cannot be adequately treated with H1 - antihistamines . In the second approach, antibodies specific for a domain of 52 amino acid residues, referred to as CεmX or M1' (M1 prime), present only on human mIgE on B cells and not on free, soluble IgE, have been prepared and are under clinical development for the treatment of allergy and asthma . An anti-M1' humanized antibody, quilizumab, is in phase IIb clinical trial . </P>

Which immunoglobin (antibody) is produced in excess during an allergic response