The worldwide prevalence of allergies has reached pandemic levels. Projections from the World Allergy Organization estimate that worldwide almost every 3rd person is affected by some sort of allergic condition such as hay fever, seasonal conjunctivitis and rhinitis, eczema, food allergy or asthma. Despite reaching such high prevalence the risks of allergic disorders are often underestimated. Allergies may result in life-threatening situations such as anaphylactic shocks leading to multiple organ failure induced death. Remarkable progress has recently been made in the understanding of allergies and the underlying molecular processes. Nevertheless, this gain of knowledge has poorly translated into clinical application so far. Most of the current treatment strategies rely on the alleviation of disease symptoms and do not directly interfere with the basic mechanism of the reaction. It is not clear why the incidence of allergic disorders has been increasing so drastically over the past few years. However, this development underlines the urgent need for new therapeutics and treatment approaches.
One of the most effective current treatment strategies is the suppression of allergic reactions by blocking the binding of soluble Immunoglobulin E (IgE) to its high-affinity receptor (FcεRI) expressed on allergic effector cells such as basophils and mast cells. The IgE:FcεRI interaction is regarded as one of the most crucial steps in the allergy cascade. Due to the slow dissociation rate of receptor-bound IgE allergic effector cells are permanently sensitized with IgE and thus ready to respond immediately upon aller- gen challenge. Namely, allergen induced cross-linking of FcεRI-bound IgE on basophils or mast cells results in the release of prestored as well as de novo synthesized inflammatory mediators. Currently the anti-IgE antibody Omalizumab represents the only therapeutically available anti-IgE compound inhibiting the interac- tion of soluble IgE with FcεRI. However, due to the high concentrations required for effective treatment and the associated financial burden Omalizumab application is restricted to a small group of severe asthma patients.
By investigating basic mechanisms underlying allergic reactions we are trying to get a better understanding of how to efficiently interfere with disease development. The ultimate goal is to find, assess and propose alternative treatment options to efficiently inhibit allergic reactions.
One of the most effective current treatment strategies is the suppression of allergic reactions by blocking the binding of soluble Immunoglobulin E (IgE) to its high-affinity receptor (FcεRI) expressed on allergic effector cells such as basophils and mast cells. The IgE:FcεRI interaction is regarded as one of the most crucial steps in the allergy cascade. Due to the slow dissociation rate of receptor-bound IgE allergic effector cells are permanently sensitized with IgE and thus ready to respond immediately upon aller- gen challenge. Namely, allergen induced cross-linking of FcεRI-bound IgE on basophils or mast cells results in the release of prestored as well as de novo synthesized inflammatory mediators. Currently the anti-IgE antibody Omalizumab represents the only therapeutically available anti-IgE compound inhibiting the interac- tion of soluble IgE with FcεRI. However, due to the high concentrations required for effective treatment and the associated financial burden Omalizumab application is restricted to a small group of severe asthma patients.
By investigating basic mechanisms underlying allergic reactions we are trying to get a better understanding of how to efficiently interfere with disease development. The ultimate goal is to find, assess and propose alternative treatment options to efficiently inhibit allergic reactions.