Single nucleotide polymorphisms of IL-2, but not IL-12 and IFN-γ, are associated with increased susceptibility to chronic spontaneous urticaria.
BACKGROUND
A clear picture of interaction of Th1/Th2 cytokines in pathogenesis of chronic spontaneous urticaria (CSU), remains elusive. Impaired IFN-γ production and decreased levels of IL-2 have been reported. The aim of this study was to evaluate the association of Th1 cytokines; IL-2, IL-12 and IFN-γ polymorphisms with CSU.


METHODS
90 patients with CSU and 140 age-sex matched subjects were included in this study. DNA samples were evaluated through PCR-SSP assay in order to detect single nucleotide polymorphisms of IL-12 (A/C -1188) or (rs3212227), IFN-γ (A/T UTR5644) or (rs2069717) and IL-2 (G/T -330 and G/T +166) or (rs2069762 and rs2069763).


RESULTS
G allele at -330 at promoter region of IL-2 gene was overrepresented in CSU. Heterozygotes (GT) at this locus and heterozygotes at +166 of IL-2 gene (GT) were more prevalent in CSU group. Additionally, the haplotype GT for loci -330 and +166 of IL-2 gene was powerfully associated with CSU (OR (95%CI)=57.29 (8.43-112.7)).


CONCLUSIONS
SNP at position -330 and +166 of IL-2 gene are differently expressed in CSU. The haplotype GT of IL-2 at -330 and +166 might confer vulnerability to a number of immunological disorders in Iranian region.
Department of Pediatrics, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
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M
Movahedi
Department of Allergy and Clinical Immunology, Shahid Bahonar Hospital, Alborz University of Medical Sciences, Karaj, Iran.
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M
Tavakol
Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran; Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
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F
Rahmani
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
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AA
Amirzargar
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
A Z
AZ
Bidoki
Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
K
K
Heidari
Department of Pediatrics, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
M
M
Gharagozlou
Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
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A
Aghamohammadi
Department of Allergy and Immunology, Rasool-e-Akram Hospital, Iran University of Medical Sciences, Tehran, Iran.
M
M
Nabavi
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
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S
Soltani
Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran; Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Boston, MA, USA. Electronic address: rezaei_nima@tums.ac.ir.
N
N
Rezaei
D016022:Case-Control Studies; D002908:Chronic Disease; D005260:Female; D005787:Gene Frequency; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics*; D018664:Interleukin-12 / Q000235:genetics*; D007376:Interleukin-2 / Q000235:genetics*; D007492:Iran; D008297:Male; D020641:Polymorphism, Single Nucleotide; D014581:Urticaria / Q000235:genetics*
D007376:Interleukin-2; D018664:Interleukin-12; D007371:Interferon-gamma
Chronic spontaneous urticaria; Interferon gamma; Interleukin 12; Interleukin 2; Single nucleotide polymorphisms