Lack of association between atopic eczema/dermatitis syndrome and polymorphisms in the promoter region of RANTES and regulatory region of MCP‐1

Background: Chemokines play an important role in the pathophysiology of atopic eczema/dermatitis syndrome (AEDS) and allergy. Recently polymorphisms in the promoter region of RANTES (regulated on activation normal T cell expressed and secreted) and in the gene regulatory region of MCP‐1 (monocyte ch...

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Published inAllergy (Copenhagen) Vol. 57; no. 2; pp. 160 - 163
Main Authors Kozma, G. T., Falus, A., Bojszkó, Á ., Krikovszky, D., Szabó, T., Nagy, A., Szalai, C.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Science, Ltd 01.02.2002
Blackwell
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Summary:Background: Chemokines play an important role in the pathophysiology of atopic eczema/dermatitis syndrome (AEDS) and allergy. Recently polymorphisms in the promoter region of RANTES (regulated on activation normal T cell expressed and secreted) and in the gene regulatory region of MCP‐1 (monocyte chemoattractant protein‐1) have been found, which increase the expression of these chemokines. The − 403A allele of the RANTES promoter region was found associated with AEDS in German children. We investigated whether the presence of these polymorphisms was associated with AEDS or allergy in Hungarian children. Methods:  One hundred and twenty‐eight children with AEDS, 102 allergic children without AEDS and 303 children of comparable ages without allergic disorders were screened for genotype with a PCR‐based assay. Results: There were no significant differences in the frequency of these polymorphisms, or in the distribution of genotypes between the groups. The total IgE concentration, the white blood cell count and the blood eosinophil cell count did not differ between the genotypes. Conclusion: In this cohort of Hungarian children there was no association between − 28G, and − 403A alleles in the RANTES promoter, − 2518G polymorphism in the distal regulatory region of the MCP‐1 and AEDS, or allergy.
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ISSN:0105-4538
1398-9995
DOI:10.1034/j.1398-9995.2002.1s3361.x