Confirmation of Genetic Linkage to Atopy on Chromosome 11 in Sixty-Four Nuclear Families and Estimation of Heterogeneity

Young, R. P.; Lynch, JR; Cookson, W. O. C. M.; Hopkin, J. M.

doi:10.1042/cs079019p

Cited by 3 publications

(2 citation statements)

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“…Total and specific IgE titres were determined by a solid-phase immunoassay (Phadezym IgE EIA and Phadezym RAST, Pharmacia Ltd, Milton Keynes, U.K.) using D. pterony.ssinus, mixed grasses, mixed moulds and mixed epithelium antigen discs. We designated children as atopic according to our previous criteria [5,6]; a skin weal of 2 mm or more than control to any antigen, or a RAST score of 1 or more (>0 35 RU/mi) to any antigen, or an elevated total IgE (geometric mean plus one standard deviation as recommended by Pharmacia) [21,22]. An individual was designated as sensitive to house dust mites (HDM-atopic) if they had a RAST score of I or more and/or a skin prick weal of 2 mm or more than control, to D. pteronyssinus.…”

Section: Ige Phenotypingmentioning

confidence: 99%

“…This has been confirmed in a study of 64 young and representative nuclear families in which the I Iq atopy locus was shown Correspondence: Dr R. P. Young. Asthma Genetics Group, Nuificld Dcpartnienl of Clinical Medicine, John Radciiffe Hospital, Oxford OX3 9DU, U.K. to underly atopy in these families [6]. Thus, individuals wilh this inherited propensity to exaggerated IgE responses may become sensitized to a range of common environmental allergens following exposure.…”

Section: Introduetionmentioning

confidence: 99%

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House dust mite sensitivity: interaction of genetics and allergen dosage

Young

Hart

Merrett³

et al. 1992

Clin Experimental Allergy

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Pairwise analysis of siblings from 21 families showed that house dust mite (HDM) sensitive children were exposed to higher concentrations of Der p I allergen in their mattress (P = 0.005) and bedding (P = 0.04), but not bedroom floor (P = 0.33), than their atopic sibling who was not sensitive to HDM antigens. There was no difference in the exposure to HDM numbers/100 mg of dust in the mattress (P = 0.61) or bedroom floors (P = 0.09). In contrast, pairwise analysis of siblings from 15 families showed that HDM sensitive children were not exposed to significantly different concentrations of Der p I in the mattress (P = 0.96), bedding (P = 0.11) or bedroom floor (P = 0.70) nor HDM numbers/100 mg of dust in the mattress (P = 0.12) and bedroom floor (P = 0.98) than their non-atopic siblings. These findings were identical when absolute allergen load was compared in these pairs. Genetic linkage studies in these families suggest the tendency to atopic IgE responses is conferred by a putative atopy locus on chromosome 11q. These results together suggest that differences in allergen levels in beds, among siblings with a comparable genetic tendency to atopy, play a significant role in determining the development of HDM allergy.

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Section: Ige Phenotypingmentioning

confidence: 99%

Section: Introduetionmentioning

confidence: 99%