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IgE was simultaneously discovered in 1966 and 1967 by two independent groups: [12] by Kimishige Ishizaka and his wife Teruko Ishizaka at the Children's Asthma Research Institute and Hospital in Denver, Colorado, [13] and by Gunnar Johansson and Hans Bennich in Uppsala, Sweden. [14] Their joint paper was published in April 1969. [15]
It can be distinguished from autosomal dominant hyper-IgE (STAT3 deficiency) because people with DOCK8 deficiency have low levels of IgM and an impaired secondary immune response. [3] IgG and IgA levels are usually normal to high.
Low air quality from environmental factors such as traffic pollution or high ozone levels [46] has been associated with both asthma development and increased asthma severity. [47] Over half of cases in children in the United States occur in areas when air quality is below the EPA standards. [ 48 ]
Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years. [62] The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 10. [63]
The fundamental problem in asthma appears to be immunological: young children in the early stages of asthma show signs of excessive inflammation in their airways. Epidemiological findings give clues as to the pathogenesis : the incidence of asthma seems to be increasing worldwide, and asthma is now very much more common in affluent countries.
The RAST is a radioimmunoassay test to detect specific IgE antibodies to suspected or known allergens for the purpose of guiding a diagnosis about allergy. [10] [11] IgE is the antibody associated with Type I allergic response: for example, if a person exhibits a high level of IgE directed against pollen, the test may indicate the person is allergic to pollen (or pollen-like) proteins.
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