Gene polymorphisms of interleukin-4, interleukin-10 and transforming growth factor-beta in Graves’ disease

Khalilzadeh, Omid; Anvari, Mehdi; Momen-Heravi, Fatemeh; Esteghamati, Alireza; Rashidi, Armin; Mahmoudi, Mahdi; Nikbin, Behrouz; Amirzargar, Aliakbar

doi:10.1007/s10238-009-0078-5

Cited by 19 publications

(17 citation statements)

References 40 publications

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“…The -238A/G polymorphism did not have a significant association with GD in our series. One reason for this inconsistency with previous reports may be related to ethnic differences, as we have previously demonstrated for other cytokine gene polymorphisms [19]. Sample size difference between studies is another potential explanation.…”

Section: Discussionmentioning

confidence: 69%

Graves’ disease and gene polymorphism of TNF-α, IL-2, IL-6, IL-12, and IFN-γ

Anvari

Khalilzadeh

Esteghamati

et al. 2010

Endocr

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The role of genetic factors in the pathogenesis of Graves' disease (GD) is not clear. The purpose of this study was to investigate the association between single nucleotide polymorphisms in pro-inflammatory cytokine genes and GD in Iranian patients. A case-control hospital-based study was carried out on 107 GD patients and 140 healthy controls. Cytokine typing was performed by polymerase chain reaction with sequence-specific primers (PCR-SSP) assay. The allele and genotype frequencies of the following cytokine genes were determined: TNF-α (-308A/G, -238A/G), IL-2 (-330T/G, +166G/T), IL-6 (-174C/G, A/G nt565), IL-12 (-1188A/C), and IFN-γ (UTR 5644A/T). The following alleles and genotypes were significantly overrepresented in patients: TNF-α -308A allele (P < 0.01) and AA genotype (P < 0.05), IL-2 -330G allele (P < 0.01) and GG genotype (P < 0.01), IL-6 -174C allele (P < 0.01) and CC genotype (P < 0.01), IL-12 -1188C allele (P < 0.01) and CC genotype (P < 0.01), IFN-γ UTR5644T allele (P < 0.01) and TT genotype (P < 0.01). In conclusion, this is the first study to show a significant association between GD and IL-2 -330G, IL-12 -1188C, and IFN-γ UTR 5644T alleles. Our results support the hypothesis that polymorphism in pro-inflammatory cytokines might be involved in predisposition to GD.

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Section: Discussionmentioning

confidence: 69%

Graves’ disease and gene polymorphism of TNF-α, IL-2, IL-6, IL-12, and IFN-γ

Anvari

Khalilzadeh

Esteghamati

et al. 2010

Endocr

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“…There were three reported studies of a genetic association of the two shared SNPs (rs1800896 and rs1800872) with GD susceptibility from Iran, Taiwan, and the UK [9,13,14]. All three studies were independent, and the data were in Hardy-Weinberg equilibrium.…”

Section: Meta-analysis Of Snps and Gdmentioning

confidence: 96%

“…The gene encoding IL-10 is located at Chr.1q32.2. A number of previous studies have identified a significant association between autoimmune diseases and three of the most characterized singlenucleotide polymorphisms (SNPs) in the promoter region of IL-10, positions -1082 A/G (rs1800896), -819 T/C (rs1800871), and absolute-link -592 A/C (rs1800872) [9].…”

Section: Introductionmentioning

confidence: 99%

“…The rs1800896 (A-1082G) and rs1800872 (A-592C) polymorphisms have been revealed to may be genetic risk factors for GD [9].To investigate the relationship between the IL-10 gene and susceptibility to GD, we performed two independent case-control association studies with Chinese GD patients targeting SNP genotyping and haplotype analysis. We also performed a meta-analysis combining current and previously reported data to evaluate the effect of the two polymorphisms on the patient susceptibility to GD.…”

Section: Introductionmentioning

confidence: 99%

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An association of interleukin-10 gene polymorphisms with Graves’ disease in two Chinese populations

et al. 2011

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Graves' disease (GD) is a common autoimmune disorder with a genetic predisposition. The cytokine interleukin-10 (IL-10) has a central role in mediating inflammation, which may affect the outcome of the patients with GD. To elucidate the impact of IL-10 gene polymorphisms, we performed a two-stage case-control association study of five single-nucleotide polymorphisms (SNPs) within the IL-10 gene as well as a meta-analysis of two SNP's rs1800896 and rs1800872 covering three previous studies from Iran, Taiwan, and the United Kingdom. The five SNPs were genotyped by SNPstream Genotyping and Taqman PCR. There was a significant increase of G allele of rs1800896 in the two cohorts (P (allele) = 2.6 × 10(-4) and 0.0082 for cohort Shanghai and Xiamen, respectively) compared with the controls. The meta-analysis showed the risk-increasing effects for the G allele of rs1800896 in GD (OR = 1.88; P < 0.00001). The allele and haplotype analysis results suggested that the polymorphisms of IL-10 were associated with GD susceptibility in the Chinese population.

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“…It may be worth noting here that, clinically, the role of IL10 for the pathogenesis of Graves' disease can also be suspected by studies on IL10 gene polymorphisms (Khalilzadeh et al 2010) and on serum IL10 concentrations in patients with autoimmune thyroid diseases (Takeoka et al 2004). …”

Section: Cd25mentioning

confidence: 99%

Interleukin 10 deficiency attenuates induction of anti-TSH receptor antibodies and hyperthyroidism in a mouse Graves' model

Ueki¹,

Abiru²,

Kawagoe³

et al. 2011

Journal of Endocrinology

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Experimental Graves'-like hyperthyroidism can be induced in susceptible mouse strains by repetitive immunizations with recombinant adenovirus expressing the human full-length TSH receptor (TSHR) or its A-subunit. Previous studies have shown that splenocytes from immunized mice produce interferon (IFN)-g and interleukin (IL) 10 in response to antigen stimulation in an in vitro T cell recall assay. Although IFN-g is now well known to be essential for disease induction, the role(s) played by IL10 are unknown. Therefore, this study was conducted to clarify the significance of endogenous IL10 in the pathogenesis of experimental Graves' disease using IL10 deficient (IL10 K/K ) mice. Our results show that T cell response was augmented when estimated by their antigen-specific secretion of the key cytokine IFN-g, but B cell function was dampened, that is, anti-TSHR antibody titers were decreased in IL10 K/K mice, resulting in a lower incidence of Graves' hyperthyroidism (54% in IL10 C/C vs 25% in IL10). Thus, in addition to IFN-g, these data clarified the role of IL10 for optimizing anti-TSHR antibody induction and eliciting Graves' hyperthyroidism in our Graves' mouse model.

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Gene polymorphisms of interleukin-4, interleukin-10 and transforming growth factor-beta in Graves’ disease

Cited by 19 publications

References 40 publications

Graves’ disease and gene polymorphism of TNF-α, IL-2, IL-6, IL-12, and IFN-γ

Graves’ disease and gene polymorphism of TNF-α, IL-2, IL-6, IL-12, and IFN-γ

An association of interleukin-10 gene polymorphisms with Graves’ disease in two Chinese populations

Interleukin 10 deficiency attenuates induction of anti-TSH receptor antibodies and hyperthyroidism in a mouse Graves' model

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