Dominant Inheritance of Atopic Immunoglobulin-E Responsiveness

Cookson, W. O. C. M.; Hopkin, Julian M.

doi:10.1016/s0140-6736(88)90286-3

Cited by 165 publications

(74 citation statements)

References 17 publications

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“…Longstanding elevated levels of interleukin-4 may have induced excessive production of polyclonal immunoglobulin E which was directed partly against inhaled allergens. As excessive immunoglobulin E production, which has been shown to be hereditary [21], appears to play a role, we speculate that only children with an atopic predisposition demonstrate an association between Toxocara infection and allergic manifestations.…”

Section: Discussionmentioning

confidence: 85%

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Relationship between allergic manifestations and Toxocara seropositivity: a cross-sectional study among elementary school children

Buijs¹,

Borsboom²,

Renting³

et al. 1997

Eur Respir J

134

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Toxocara (the cause of visceral larva migrans in humans) and allergy have in common both elevated immunoglobulin E (IgE) levels and eosinophilia. In the present study, we investigated: 1) associations between Toxocara seropositivity and allergic manifestations; 2) risk factors for Toxocara infection; and 3) differences in Toxocara seroprevalence, allergic manifestations and the associations between these two, in children from urban and rural environments.Blood samples from 1,379 Dutch urban and rural elementary schoolchildren, were examined for Toxocara antibodies, eosinophil numbers, total IgE concentrations, and the occurrence of inhaled allergen-specific IgE. Questionnaires investigating respiratory health and putative risk factors for infection were completed.It was found that 8% of the children had Toxocara antibodies, occurring significantly less often in females than in males. The means of total serum IgE levels and blood eosinophils were significantly higher in the Toxocara-seropositive than in the seronegative group. Allergic asthma/recurrent bronchitis was found in 7% of the children, allergic reaction on animal contact in 4%, and IgE to at least one inhaled allergen in 16%. These variables were associated with Toxocara seroprevalence. Inhaled allergen-specific IgE and asthma/recurrent bronchitis occurred significantly less often in rural than in urban areas, and significantly less often among girls than among boys. Furthermore, occurrence of allergen-specific IgE increased significantly with age. No association existed between Toxocara seroprevalence and assumed risks, i.e. contact with pet animals and public playgrounds.In conclusion, our results indicate that allergic manifestations occur more often in Toxocara-seropositive children. A relationship with an already existing allergic condition is plausible. Eur Respir J 1997; 10: 1467-1475 Recent investigations suggest an increasing prevalence of childhood asthma [1,2]. Children at risk are those with an atopic constitution [3,4]. The age at which allergy becomes manifest depends mainly on the degree of exposure to inhaled allergens, the most obvious being that to house dust mite (Dermatophagoides pteronyssinus) allergen [5]. Frequent exposure to allergens may accelerate expression of allergic symptoms at a young age [6]. Various products of biological origin, such as antigens derived from parasitic worms, have polyclonal B ε -cell-activating properties, and can, thereby, induce high serum total immunoglobulin E (IgE) concentrations [7,8].Toxocara spp., intestinal parasites of dogs and cats, may spend part of their life cycle in noncompatible hosts, including humans. Toxocara is endemic in the Netherlands. About 8% of the children have antibodies to this roundworm [9]. Eggs are passed on the soil with dog/cat faeces; the infection, therefore, is soil transmitted. Larvae, hatched in the intestine from ingested eggs, migrate to the body tissues, such as liver and lungs. In noncompatible hosts, the larvae do not develop, and may survive as such...

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Section: Discussionmentioning

confidence: 85%

“…excessive IgE production, eosinophilia, and respiratory complaints [1,3,13]. Excessive IgE production after contact with IgE-stimulating agents is an inherited phenomenon [21]. Young children with an atopic condition risk development of allergic asthma during growth [22].…”

Section: Discussionmentioning

confidence: 99%

Relationship between allergic manifestations and Toxocara seropositivity: a cross-sectional study among elementary school children

Buijs¹,

Borsboom²,

Renting³

et al. 1997

Eur Respir J

134

View full text Add to dashboard Cite

show abstract

“…and Hay Fever To examine the relationship between resent a bias in perception rather than a biologic difference in susceptibility (6,28). The lack of a significant, positive correlation with age in reported cumulative prevalence may be due to the fact that most individuals develop asthma and hay fever before 20 yr of age or to secular increases of incidence with time or to increased forgetting or denial of disease with age (29).…”

Section: Bivariate Model For Asthma/wheezingmentioning

confidence: 99%

Genetics of Asthma and Hay Fever in Australian Twins

Duffy¹,

Martin²,

Battistutta³

et al. 1990

Am Rev Respir Dis

471

277

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“…Using complex segregation analysis techniques for studying IgE concentrations in 173 families, Gerard and colleagues concluded that the regulatory locus for IgE occupied two alleles, with the dominant allele suppressing persistently high levels of IgE 19 . The observation that 90% of atopic asthmatics in 239 members of forty nuclear families had an atopic parent led Cookson and Hopkin to suggest a dominant model of inheritance for propensity to produce an exaggerated IgE response 20 . Other Mendelian models proposed have included autosomal recessive inheritance, autosomal dominant inheritance with incomplete penetrance, codominance, and dominant inheritance through the maternal line 21 .…”

Section: Segregation Analysismentioning

confidence: 99%

Itch, Sneeze and Wheeze: The Genetics of Atopic Allergy

Sheikh¹

2002

J R Soc Med

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In many developed countries over one-®fth of the population are affected by one or more atopic allergic disorders. Several time-trend studies indicate that the prevalence and severity of eczema, rhinitis, and asthma is rapidly increasing 1±3 ; and this observation, coupled with the widespread geographical variations in disease prevalence noted by the International Studies of Asthma and Allergies in Childhood, points to the strong contribution of environment to the aetiology 4 . However, the tendency of atopic allergic conditions to cluster both within individuals and within families suggests that genetic factors are also important.Asthma is a condition characterized by reversible air¯ow obstruction and lower airway hyper-responsiveness, which results in episodic cough, wheeze and shortness of breath 5 . In¯ammation of the nasal passages, manifesting as sneezing, nasal blockage and itchy rhinorrhoea, is the symptom complex known as rhinitis 6 . Eczema is the commonest cause of dermatitis in developed countries and affects approximately 20% of the general population 7 . The distribution of eczematous lesions varies with age, the face and trunk being most affected in infants whereas the¯exor aspects of the limbs are typically affected in older children and adults. Advances in our understanding of the immunobiology of these disorders have shown them to have a common pathophysiological basisÐan exaggerated and inappropriate IgE-mediated in¯ammation in response to allergen exposureÐreferred to as atopy 8 . The absence of objective and reliable criteria for de®ning either atopy or the atopic allergic conditions (eczema, rhinitis and asthma) has been and continues to be a major obstacle to establishing the genetic basis of atopic disorders.This review is based in the main on articles retrieved by searching Medline, EMBASE and OMIM (Online Mendelian Inheritance in Man) electronic databases. Key websites of possible relevance were also searched 9 , including those of the British Society for Human Genetics 10 , the European Society for Human Genetics 11 , and the Human Mutation Database 12 . Allergy and genetic texts were consulted, and the analysis was helped by personal contacts with several experts on human genetics. FAMILIAL STUDIES Evidence for familial clusteringAnecdotal evidence for familial clustering of atopic disorders dates back to the early twentieth century 13 . More rigorous evidence emerged in the latter half of the century, when many studies showed that relatives of atopic patients had a higher prevalence of atopic allergic disorders than did relatives of matched non-atopic patients 14 . Research subsequently revealed that atopic individuals and couples were substantially more likely than non-atopics to give birth to children with one or more atopic disorders 15 . Although these ®ndings provided strong and consistent evidence for the importance of shared familial characteristics, they were in themselves insuf®cient to prove genetic causation.Studies in twins are a good way to disentangle genetic and enviro...

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Dominant Inheritance of Atopic Immunoglobulin-E Responsiveness

Cited by 165 publications

References 17 publications

Relationship between allergic manifestations and Toxocara seropositivity: a cross-sectional study among elementary school children

Relationship between allergic manifestations and Toxocara seropositivity: a cross-sectional study among elementary school children

Genetics of Asthma and Hay Fever in Australian Twins

Itch, Sneeze and Wheeze: The Genetics of Atopic Allergy

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