Atopy

Atopy is the tendency to produce an exaggerated immunoglobulin E (IgE) immune response to otherwise harmless substances in the environment. Allergic diseases are clinical manifestations of such inappropriate, atopic responses. Atopy may have a hereditary component, although contact with the allergen or irritant must occur before the hypersensitivity reaction can develop (characteristically after re-exposure). Maternal psychological trauma in utero may also be a strong indicator for development of atopy. The term atopy was coined by Arthur F. Coca and Robert Cooke in 1923. Many physicians and scientists use the term "atopy" for any IgE-mediated reaction (even those that are appropriate and proportional to the antigen), but many pediatricians reserve the word "atopy" for a genetically mediated predisposition to an excessive IgE reaction. The term is from Greek ἀτοπία meaning "the state of being out of place", "absurdity". Atopic sensitization is considered IgE positivity or prick test positivity to any common food- or air-borne allergen. Atopic conditions are considered: atopic dermatitis, allergic rhinitis (hay fever), allergic asthma, atopic keratoconjunctivitis. The likelihood of having asthma, rhinitis and atopic dermatitis together is 10 times higher than could be expected by chance. Atopy is more common among individuals with a number of different conditions, such as eosinophilic esophagitis and non-celiac gluten sensitivity. Allergic reactions can range from sneezing and rhinorrhoea to anaphylaxis and even death. In an allergic reaction, initial exposure to an otherwise harmless exogenous substance (known as an allergen) triggers the production of specific IgE antibodies by activated B cells. These IgE antibodies bind to the surface of mast cells via high-affinity IgE receptors, a step that is not itself associated with a clinical response. However, upon re-exposure, the allergen binds to membrane-bound IgE which activates the mast cells, releasing a variety of mediators.