The association between IgE, asthma, and atopy is well known. Although interleukins 4 and 13 play a prominent role in the development of airways hyperresponsiveness, they are also involved in induction of the primary IgE immune response and promote transcription of IgE constant region genes in B cells. The role of interleukin 4 in the secondary or anamnestic response is less clear. IgE mediates inflammation via two receptors, FcεRI and FcεRII, which are high- and low-affinity receptors for IgE, respectively. Once bound, cross-linking of IgE molecules by antigen promotes the release of mediators capable of inducing bronchospasm and recruitment of other inflammatory cells. The development of an anti-IgE antibody using hybridoma techniques resulted in the development of rhuMAb-E25, or omalizumab. This monoclonal antibody has been shown in clinical trials to reduce the early and late asthmatic responses to inhaled allergens and dramatically reduce free IgE levels. Although rhuMAb-E25 is a promising therapy in the treatment of asthma, especially in moderate to severe asthmatics, the optimal route of administration (intravenous or subcutaneous), dose, and frequency still need to be determined. The use of rhuMAb-E25 would seem to be most beneficial in those patients with very high IgE levels; however, the risk of developing immune complex-mediated disease in such patients needs to be clarified with further studies. In addition to rhuMAb-E25, future asthma therapies will undoubtedly target the cytokines intimately involved in the early and late asthmatic responses.
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Critical Care and Intensive Care Medicine