Promoter polymorphisms in the chromosome 5 gene cluster in asthma and atopy

Rosenwasser, Lanny J.; Klemm, Dwight J.; Dresback, J.; Inamura, Hiroaki; Mascali, J J; Klinnert, Mary D.; Borish, Larry

doi:10.1111/j.1365-2222.1995.tb00428.x

Cited by 502 publications

(362 citation statements)

References 16 publications

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“…Our results indicate a significant but weak effect of at least 10 strongly linked polymorphisms in the IL4 gene on the expression of the asthma phenotype and increased serum IgE levels. These findings are in accordance with previously published results, in which C-589T linked the polymorphism in T-589 to increased total serum IgE levels in a group of 44 asthmatic patients 6 and fatal/near-fatal asthma, as well as "probable" asthma. 23,24 In contrast, a large study conducted in 1128 children from Australia and England could not find associations between the C-589T polymorphism and atopic phenotypes, 25 except for a weak association with specific IgE against house dust mites in Australian, but not in English, children.…”

Section: Discussionsupporting

confidence: 93%

“…The IL4 gene has been sequenced in full, 5 and a polymorphism (C-589T) in the IL4 promoter region has been identified. 6 A second single nucleotide polymorphism (SNP; C-33T) was reported recently in the 5′ untranslated region of the gene. 7 Furthermore, an association between C-589T and total serum IgE levels, 6 asthma, 8 and atopic dermatitis 9 was suggested in some studies but could not be confirmed by others.…”

mentioning

confidence: 99%

“…6 A second single nucleotide polymorphism (SNP; C-33T) was reported recently in the 5′ untranslated region of the gene. 7 Furthermore, an association between C-589T and total serum IgE levels, 6 asthma, 8 and atopic dermatitis 9 was suggested in some studies but could not be confirmed by others. 10 Recently, we have reported a highly significant association of total serum IgE levels with a cluster of 7 tightly linked polymorphisms in the IL13 gene in 3 independent populations.…”

mentioning

confidence: 99%

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A complete screening of the IL4 gene

Kabesch¹,

Tzotcheva²,

Carr³

et al. 2003

Journal of Allergy and Clinical Immunology

107

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Section: Discussionsupporting

confidence: 93%

mentioning

confidence: 99%

mentioning

confidence: 99%

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A complete screening of the IL4 gene

Kabesch¹,

Tzotcheva²,

Carr³

et al. 2003

Journal of Allergy and Clinical Immunology

107

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“…Similarly, the protective À589T polymorphism is under-represented among CDC patients and this polymorphism is functional for enhanced IL-4 transcriptional activity. 23 Disseminated or systemic candidiasis, another form of invasive infection, is characterized by the hematogenous spread of Candida to one or multiple organs. 21 Systemic candidiasis is a life-threatening infection, with the overall prognosis comparable to septic shock with multiple organ failure.…”

Section: Types Of Candidiasismentioning

confidence: 99%

Genetic analysis of innate immunity in resistance to Candida albicans

2004

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Systemic candidiasis is a significant cause of nosocomial infections and the mechanisms of defense against Candida albicans in humans remain poorly understood. Studies in animal models have demonstrated the importance of innate immunity in controlling the response to infection. Although Th1 cytokines have been shown to direct the overall outcome of infection, the precise role of the Th1/Th2 response and, more generally, the adaptive immune response as a whole, in systemic candidiasis, appears to apply mainly to the development of resistance to reinfection. A genetic approach to the identification of host factors regulating pathogenesis and susceptibility to C. albicans infection has been used in humans and in mouse models of infection. Mouse mutants bearing experimentally induced mutations in specific genes have provided a systematic tool for directly assessing the role of individual proteins in C. albicans susceptibility. Inbred mouse strains have been valuable in showcasing the spectrum of naturally occurring variations in initial susceptibility to infection, and type of disease developed. Crosses between resistant and susceptible strains have led to the detection of additional gene effects affecting innate immunity. Of particular interest is the major effect of a naturally occurring loss-of-function mutation in the C5 complement component that has become fixed in many inbred strains. These and other studies have shown that both a functional complement pathway and robust inflammatory response are critical for resistance to C. albicans.

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“…Rosenwasser et al (54) showed that an IL4 promoter polymorphism, a C to T change at position )590 bp, is associated with elevated serum IgE levels in atopic families.…”

Section: Ige Responsivenessmentioning

confidence: 99%