Type I Hypersensitivity

Type I hypersensitivity or immediate hypersensitivity is an allergic reaction provoked by reexposure to a specific type of antigen referred to as an allergen.[1] Exposure may be by ingestion, inhalation, injection, or direct contact. Pathophysiology The difference between a normal immune response and a type I hypersensitive response is that in the latter plasma cells secrete IgE. This class of antibodies binds to Fc receptors on the surface of tissue mast cells and blood basophils.[2] Mast cells and basophils coated by IgE are "sensitized." Later exposure to the same allergen, cross-links the bound IgE on sensitized cells resulting in degranulation and the secretion of pharmacologically active mediators such as histamine, leukotriene (LTC4 and LTD4), and prostaglandin that act on the surrounding tissues. The principal effects of these products are vasodilation and smooth-muscle contraction. Treatment and prognosis Treatment usually involves epinephrine, antihistamines, and corticosteroids. If the entire body gets involved, then anaphylaxis can take place. Examples Some examples: • • • • • • • • • •

Allergic asthma Allergic conjunctivitis Allergic rhinitis ("hay fever") Anaphylaxis Angioedema Urticaria (hives) Eosinophilia Penicillin Cephalosporin Food allergy

Prevention In the present methods, the anti-IgE antibody binds to circulating or serum IgE and/or IgE bound to B-cells, but preferably does not bind to IgE bound to mast cells or basophils, as this may cause crosslinking. In addition, the anti-IgE antibody also prevents the binding of IgE to the low-affinity IgE receptor (FcεRll) on B cells and antigen presenting cells such as dendritic cells, thereby further reducing the production of allergen-specific IgE by B cells.