Analysis of IL-2 and IL-6 binding to peripheral blood lymphocytes in Graves disease: Relationship with disease activity

Corrales, J. J.; Órfão, Alberto; López, Á.; Mories, M.T.; Jm, Miralles García; Ciudad, Juana

doi:10.1002/(sici)1097-0320(19970615)30:3<118::aid-cyto2>3.0.co;2-h

Cited by 14 publications

(8 citation statements)

References 31 publications

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“…Considering its important role in growth and differentiation of lymphocytes, IL-6 might contribute to the promotion of thyroid receptor antibody synthesis during the course of GD [8,24,25]. The observation that the -174C allele and the CC genotype had higher frequencies in our patients is in contrast with a previous study in Polish- Caucasian patients [26].…”

Section: Discussioncontrasting

confidence: 98%

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: Discussioncontrasting

confidence: 98%

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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“…Moreover, we have failed to show a relationship between the differences of IL-6/sIL-6R concentrations and the presence of circulating TRAb or TPOAb, suggesting that the activation of the IL-6 system may be independent of thyroid function and of humoral reactions in the thyroid. A correlation between increased numbers of peripheral T-and B-cells binding IL-6, and serum TRAb activity has been found in hyperthyroid untreated GD patients in a recent study (29), suggesting that IL-6 is involved in both the immunological and the hormonal abnormalities of the disease. Heuer et al (30) studied the patterns of cytokine mRNA expression in GD, HT and non-autoimmune disorders and observed mainly quantitative differences, i.e.…”

Section: Discussionmentioning

confidence: 88%

Serum concentrations of proinflammatory cytokines in Graves' disease: effect of treatment, thyroid function, ophthalmopathy and cigarette smoking

Salvi

Pedrazzoni

Girasole

et al. 2000

European Journal of Endocrinology

129

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Objective: In the present study we have measured the concentrations of interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b) and IL-1 receptor antagonist (IL-1Ra) in the serum of patients with Graves' disease (GD). By multivariate analysis, we have evaluated the effect of antithyroid treatment, thyroid function, the presence or absence of active thyroid-associated ophthalmopathy (TAO), the patient's smoking habits and the relation to circulating anti-thyrotropin (TSH) receptor (TRAb) and anti-thyroperoxidase antibodies (TPOAb). Subjects: We studied 84 GD patients, 51 untreated and 33 receiving methimazole (MMI) therapy. Twenty-three (45%) untreated patients and 18 (54%) patients on MMI had active TAO. We also studied 67 normal subjects as controls. Thirty-one GD patients (43%) and 16 controls (36%) were smokers. Results: Serum IL-6 concentrations were signi®cantly higher in both untreated patients (P < 0.001) and treated patients (P < 0.006), when compared with controls. Serum sIL-6R concentrations were signi®cantly affected by treatment (P 0:001). Serum IL-1Ra concentrations were not different in GD patients, whether treated or untreated, compared with controls. Serum IL-6 concentrations were not in¯uenced by thyroid function and there was a signi®cant interaction between treatment and the presence of active TAO (P 0:003). In hyperthyroid patients with active TAO serum, sIL-6R concentrations were signi®cantly higher than in those with inactive TAO (P 0:003). In untreated GD patients there was no signi®cant effect of thyroid function and TAO activity on the serum concentrations of TNF-a and IL-1b. Serum IL-1Ra concentrations were not affected by the presence of TAO. Smoking had no effect on serum IL-6, sIL-6R, TNF-a, IL-1b and IL-1Ra concentrations, even in the presence of an active TAO. Serum concentrations of IL-6, sIL-6R, TNF-a and IL-1b and IL-1Ra were not different in patients with and without TRAb or TPOAb, in relation to either thyroid function, TAO activity or smoking. Conclusions: Our work shows that: (i) the proin¯ammatory cytokine pattern in GD is greatly in¯uenced by antithyroid drug treatment; (ii) the increased circulating IL-6/sIL-6R concentrations observed in patients with active TAO may derive from the activation of humoral reactions in sites other than the thyroid; and, (iii) cigarette smoking has no effect on serum IL-1/IL-1Ra concentrations in TAO.

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“…CD25 expressions on the peripheral lymphocytes have been reported to increase in patients with various autoimmune disorders (9)(10)(11)14,28,29). In the patients with HD, the proportions of CD3 1 CD25 1 cells increased (12) and the CD25 1 cells were more frequent among the CD4 1 helper T cells (13).…”

Section: Discussionmentioning

confidence: 99%

Independent Involvement of CD8⁺CD25⁺Cells and Thyroid Autoantibodies in Disease Severity of Hashimoto's Disease

Watanabe

Yamamoto

Maruoka

et al. 2002

Thyroid

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Hashimoto's disease (HD) is well known as an autoimmune thyroid disease caused by the destruction of the thyroid follicles, and can be diagnosed in the subclinical stage with thyroid-specific autoantibodies. However, some patients with HD develop hypothyroidism and are treated with thyroxine (severe HD), but most do not throughout their lives (mild HD). To clarify the immunologic differences between these two groups of patients with HD, we examined serum thyroid autoantibodies (antithyroid peroxidase antibodies and antithyroglobulin antibodies), CD4+ CD25+ cells that contain regulatory T cells and activated helper T cells, and CD8+ CD25+ cells that are activated cytotoxic T cells. There was no significant difference in CD4+ CD25+ cells between these HD groups, although the proportion of CD25+ cells within CD4+ cells increased in both groups as compared to normal controls. The serum titers of the thyroid autoantibodies and the proportion of CD25+ cells within CD8+ cells were higher in patients with severe HD than in those with mild HD. There was no correlation between these two parameters, and a two-dimensional analysis with these parameters differentiated these two groups of patients with HD more clearly. These results indicate that both thyroid autoantibodies and CD8+ CD25+ cells are independently involved in the disease severity of HD and CD4+ CD25+ cells are not related to the severity of HD.

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Analysis of IL-2 and IL-6 binding to peripheral blood lymphocytes in Graves disease: Relationship with disease activity

Cited by 14 publications

References 31 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

Serum concentrations of proinflammatory cytokines in Graves' disease: effect of treatment, thyroid function, ophthalmopathy and cigarette smoking

Independent Involvement of CD8⁺CD25⁺Cells and Thyroid Autoantibodies in Disease Severity of Hashimoto's Disease

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Analysis of IL-2 and IL-6 binding to peripheral blood lymphocytes in Graves disease: Relationship with disease activity

Cited by 14 publications

References 31 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

Serum concentrations of proinflammatory cytokines in Graves' disease: effect of treatment, thyroid function, ophthalmopathy and cigarette smoking

Independent Involvement of CD8+CD25+Cells and Thyroid Autoantibodies in Disease Severity of Hashimoto's Disease

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Independent Involvement of CD8⁺CD25⁺Cells and Thyroid Autoantibodies in Disease Severity of Hashimoto's Disease