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Allergies: general

from Medical topics

Published online by Cambridge University Press:  18 December 2014

By
Mary Gregerson
Edited by
Susan Ayers ,
Andrew Baum ,
Chris McManus ,
Stanton Newman ,
Kenneth Wallston ,
John Weinman  and
Robert West
Mary Gregerson
Affiliation:
Family Therapy Institute of Alexandria
Susan Ayers
Affiliation:
University of Sussex
Andrew Baum
Affiliation:
University of Pittsburgh
Chris McManus
Affiliation:
St Mary's Hospital Medical School
Stanton Newman
Affiliation:
University College and Middlesex School of Medicine
Kenneth Wallston
Affiliation:
Vanderbilt University School of Nursing
John Weinman
Affiliation:
United Medical and Dental Schools of Guy's and St Thomas's
Robert West
Affiliation:
St George's Hospital Medical School, University of London
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Summary

Features

Allergies are a T lymphocyte cell-mediated immunity (CMI) gone awry (Zweiman, 1999). Normal CMI development usually results in a synchronous, efficacious T-helper cell (Th1) mediated protection of the human from internal disruptions or against the invasion of disease provoking foreign agents. In allergies, an over-abundance of another specific type of T-helper cell named Th2 is the abnormality (Broide, 2001). After extensive research, whether the relationship between allergies and CMI is inverse remains an experimental question. For allergies, though, the elevated presence of Th2 results in an immediate hypersensitivity called Type I.

The genetic basis of allergies is commonly accepted. Even with similar genetic risk, some persons either never get allergic symptoms or theirs disappear while others continually experience allergies. Family transmission of allergy has been acknowledged since 1920. If two parents have Type I Hypersensitivity, offspring have a 50% chance to manifest atopy, and with one parent, almost a 30% chance. These individual differences in responsivity and the interruption of Mendelian genetic transmission make psychological and behavioural treatment factors important considerations in allergies.

The immune substrate of allergies is determined both by genetics (hardware) within the Type I major histocompatibilty complex (MCI) and by learning (software), for example, histamine tissue priming (Peeke et al., 1987). Both hardware and software regulate the individual's allergic immune responsivity. The Th2 pattern is related to elevated emission of a cascade of other sequela, specifically, Immunoglobulin E (IgE), interleukins (4, 13 and 10) as well as eosinophil-laden inflammation.

Type
Chapter
Information
Cambridge Handbook of Psychology, Health and Medicine , pp. 543 - 546
Publisher: Cambridge University Press
Print publication year: 2007

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