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a Asthma
Genetics Group, University of Oxford, Nuffield Department of Medicine,
John Radcliffe Hospital, Oxford, UK, b Molecular Medicine Unit, University of Leeds, St James's
University Hospital, Leeds, UK
Correspondence to: Dr G G Anderson, Asthma Genetics Group, University of Oxford, Nuffield Department of Medicine, John Radcliffe Hospital, Oxford OX3 9DU, UK.
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Introduction |
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In the past few years considerable progress has been made in understanding the pathogenesis of allergy at the cellular and subcellular level. In particular, advances in cell biology and DNA technology have shed light on the cell interactions that are pivotal in orchestrating the inflammation underlying allergy. Although much has now been established in the cellular mechanism of allergic inflammation, the fundamental question of why some people suffer from the disease and others do not has only begun to be answered by molecular genetics, which has implicated the inheritance of several genes that predispose to the development of allergy.
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Definitions |
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Allergy comprises a group of syndromes that includes asthma,
atopic dermatitis, and hay fever, and tends to occur in familial clusters. These diseases have classically been described as caused by
an allergic response characterised by immediate hypersensitivity reactions (that is, weal and flare to intradermal allergens), increased
serum IgE, and increased
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