Association between atopy and variants of the β subunit of the high–affinity immunoglobulin E receptor

Shirakawa, Taro; Li, Airong; Dubowitz, M.; Dekker, James; Shaw, Ann E.; Faux, J. A.; Ra, Chisei; Cookson, William; Hopkin, Julian M.

doi:10.1038/ng0694-125

Cited by 398 publications

(222 citation statements)

References 50 publications

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“…The present data do not demonstrate this TNFa polymorphism to be associated with atopy as defined by skin prick test to common aeroallergens nor with abnormally high total serum IgE levels, a phenotype which was previously shown to be linked to a mutation in the gene of FcReI [23]. Although the definition of atopy was restricted to skin prick test interpretation and not based on suggestive symptoms in the present study, it is believed that not many real atopic patients who could have been skin prick test negative for the two following reasons were missed.…”

Section: Discussioncontrasting

confidence: 86%

Lack of association between adult asthma and the tumour necrosis factor α-308 polymorphism gene

Louis¹,

Leyder²,

Malaise³

et al. 2000

Eur Respir J

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Lack of association between adult asthma and the tumour necrosis factor a-308 polymorphism gene. R. Louis, E. Leyder, M. Malaise, P. Bartsch, E. Louis. #ERS Journals Ltd 2000. ABSTRACT: Tumour necrosis factor (TNF)a is a cytokine endowed with potent inflammatory properties that may contribute to airway inflammation in asthma. It has previously been shown that the single base pair polymorphism-308 (G to A substitution) in the promoter of TNFa gene results in enhanced cytokine secretion. Whether this polymorphism is associated with the presence of phenotypic expression of asthma is questioned.In this study the relative frequency of TNF1 and TNF2 alleles in a population of adult healthy subjects (n=98) and adult Caucasian asthmatics (n=95) was compared taking into account their disease severity, atopic status and their smoking habit.For the whole group of asthma the genotype frequency for 1/1, 1/2, 2/2 were 67%, 33% and 0%, respectively, and not significantly different from those found in the control group that reached 70%, 28% and 2% respectively (p>0.05). The allele frequencies in asthma were 86% and 14% for TNF1 and TNF2 respectively while the corresponding figures were 85% and 15% in the control group (p>0.05). Furthermore, subdividing asthmatics into severe forced expiratory volume in one second <60% pred), atopic or smoking patients did not show any significant association with this TNFa polymorphism.To conclude the polymorphism -308 in the promoter of the TNFa gene does not confer a susceptibility to develop asthma nor to grade its severity. Eur Respir J 2000; 16: 604±608.

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Section: Discussioncontrasting

confidence: 86%

Lack of association between adult asthma and the tumour necrosis factor α-308 polymorphism gene

Louis¹,

Leyder²,

Malaise³

et al. 2000

Eur Respir J

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“…Support for altered homeostasis in Th2 diseases finds credence in studies of mutations associated with these conditions. Allergic disease-linked polymorphisms of the IL-10 promoter, the IL-4 promoter, and the IL-4R ␣-chain have been noted, as well as polymorphisms of Fc⑀RI ␤ (27,13,14,(41)(42)(43)(44)(45)(46). It is possible that such genetic changes may prevent Th2-mediated regulation of mast cell survival and/or Fc⑀RI regulation, though such effects are unknown.…”

Section: Discussionmentioning

confidence: 99%

IL-10 Inhibits FcεRI Expression in Mouse Mast Cells

Gillespie

DeMartino

Zhu

et al. 2004

The Journal of Immunology

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FcεRI expression and function is a central aspect of allergic disease. Using bone marrow-derived mouse mast cell populations, we have previously shown that the Th2 cytokine IL-4 inhibits FcεRI expression and function. In the current study we show that the Th2 cytokine IL-10 has similar regulatory properties, and that it augments the inhibitory effects of IL-4. FcεRI down-regulation was functionally significant, as it diminished inflammatory cytokine production and IgE-mediated FcεRI up-regulation. IL-10 and IL-4 reduced FcεRI β protein expression without altering the α or γ subunits. The ability of IL-4 and IL-10 to alter FcεRI expression by targeting the β-chain, a critical receptor subunit known to modulate receptor expression and signaling, suggests the presence of a Th2 cytokine-mediated homeostatic network that could serve to both initiate and limit mast cell effector function.

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“…The association between the Fc ⑀ R1 polymorphisms in this region with atopy was also divergent in patients from different ethnic groups. 27 Environmental factors are another major component in the development of atopy in different populations. A large increase in the prevalence of atopic disease in the western countries is striking and a rural lifestyle has been shown to be protective both in Europe and Africa.…”

Section: Discussionmentioning

confidence: 99%