AffiliationThe Respiratory Sciences Center, University of Arizona, Tucson, Arizona, USA
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CitationRespir Res 2001, 2:129–132 http://respiratory-research.com/content/2/3/129
Rights© 2001 BioMed Central Ltd
Collection InformationThis item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at firstname.lastname@example.org.
AbstractThe hygiene hypothesis, as originally proposed, postulated an inverse relation between the incidence of infectious diseases in early life and the subsequent development of allergies and asthma. New evidence from epidemiological, biological and genetic studies has significantly enlarged the scope of the hypothesis. It now appears probable that environmental 'danger' signals regulate the pattern of immune responses in early life. Microbial burden in general, and not any single acute infectious illness, is the main source of these signals. The latter interact with a sensitive and complex receptor system, and genetic variations in this receptor system may be an important determinant of inherited susceptibility to asthma and allergies.
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