Abstract
The presence of reaginic antibody in the serum of allergic patients was first demonstrated by Prausnitz and Kiistner (1921) . Prausnitz passively sensitized his arm by intracutaneous injection of serum from Kustner, who was sensitive to fish. The skin sites receiving the serum gave an erythema and wheal reaction on challenge with fish extract. By 1966, the immunoglobulin classes IgG, IgM, IgA and IgD had been described and none of these classes appeared to have the capacity to sensitize human skin for the Prausnitz-Kiistner (P-K) reaction (Ishizaka _et al., 1965; Ishizaka and Ishizaka., 1966). At this time the Ishizakas (Ishizaka, Ishizaka and Hornbrook, 1966; Ishizaka and Ishizaka, 1967) reported finding a reagin rich fraction in atopic patients’ sera that remained after adsorption with antisera to known immunoglobulins and myeloma proteins. It was found that the highly purified fraction had skin sensitizing activity. Concurrently Johansson and Bennich (1967) were studying what appeared to be a biochemically unique myeloma protein. Later a similar protein was shown to be present in elevated levels in the serum of patients with allergic asthma, as well as in low levels in normal individuals. This protein was subsequently recognized to be identical to the immunoglobulin found by Ishizaka and was then officially called IgE (Bennich et al., 1968; Bennich et al., 1969).