Increased Serum Concentration of Interleukin-5 in Patients with Graves' Disease and Hashimoto's Thyroiditis

Hidaka, Yoh; Okumura, Motoshi; Shimaoka, Yuki; Takeoka, Keiko; Tada, Hayato; Amino, Nobuyuki

doi:10.1089/thy.1998.8.235

Cited by 40 publications

(27 citation statements)

References 15 publications

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“…On the other hand, a recent study shows that adipose tissue secretion of interleukin-6 is elevated in Graves' disease (36) even after restoration of euthyroidism. Some authors have found elevated cytokine concentrations in autoimmune hypothyroidism (37,38), as opposed to our finding of decreased MBL levels. In parallel to our findings, it has been shown that serum sIL-2R levels are positively modulated by thyroid hormone, mostly independently of thyroid autoimmunity (39 -41).…”

Section: P-valuescontrasting

confidence: 99%

Thyroid hormone increases mannan-binding lectin levels

Riis¹,

Hansen²,

Thiel³

et al. 2005

eur j endocrinol

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Background: Recent studies have indicated the existence of causal links between the endocrine and immune systems and cardiovascular disease. Mannan-binding lectin (MBL), a protein of the innate immune system, may constitute a connection between these fields. Methods: To test whether thyroid hormone regulates MBL levels, we studied eight patients with Graves' hyperthyroidism before and after methimazole therapy, eight healthy subjects before and after short-term experimental hyperthyroidism, and eight hypothyroid patients with chronic autoimmune thyroiditis before and after L-thyroxine substitution. Results: In all hyperthyroid patients, MBL levels were increased -median (range), 1886 ng/ml (1478 -7344) -before treatment and decreased to 954 ng/ml (312 -3222) after treatment (P ¼ 0.01, paired comparison: Wilcoxon's signed ranks test). The healthy subjects had MBL levels of 1081 ng/ml (312 -1578). Administration of thyroid hormones to these persons induced mild hyperthyroidism and increased MBL levels significantly to 1714 ng/ml (356-2488) (P ¼ 0.01). Two of the eight hypothyroid patients had undetectably low levels of MBL both before and after L-thyroxine substitution. The other six hypothyroid patients had decreased levels of MBL of 145 ng/ml (20-457) compared with 979 ng/ml (214 -1533) after L-thyroxine substitution (P ¼ 0.03, paired comparison: Wilcoxon's signed ranks test). Conclusion: Our data show that thyroid hormone increases levels of MBL. MBL is part of the inflammatory complement system, and this modulation of complement activation may play a role in the pathogenesis of a number of key components of thyroid diseases.

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Section: P-valuescontrasting

confidence: 99%

Thyroid hormone increases mannan-binding lectin levels

Riis¹,

Hansen²,

Thiel³

et al. 2005

eur j endocrinol

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“…Wahrenberg et al (24) have reported that adipose tissues from these individuals release several-fold higher levels of IL-6 than do similar tissues from control subjects. Circulating IL-6 levels have also been found to be elevated in Graves' disease (17)(18)(19)(20)(21)(22). Moreover, treatment of thyrotoxicosis fails to normalize these levels, suggesting strongly that they are a consequence of the underlying autoimmune process.…”

Section: Discussionmentioning

confidence: 99%

“…Among these, IL-6 has generated considerable interest because it has been implicated in human autoimmune diseases and multiple myeloma (15,16). IL-6 and soluble IL-6R, like several other important cytokines, have been found to be elevated in patients with Graves' disease (17)(18)(19) and those with TAO (20 -23). IL-6 protein can be detected in s.c. fat in these patients (24).…”

Section: Il-1␤ Induces Il-6 Expression In Human Orbital Fibroblastsmentioning

confidence: 99%

IL-1β Induces IL-6 Expression in Human Orbital Fibroblasts: Identification of an Anatomic-Site Specific Phenotypic Attribute Relevant to Thyroid-Associated Ophthalmopathy

Chen

Tsui

Smith

2005

The Journal of Immunology

122

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Human orbital fibroblasts exhibit a unique inflammatory phenotype. In the present study, we report that these fibroblasts, when treated with IL-1β, express high levels of IL-6, a cytokine involved in B cell activation and the regulation of adipocyte metabolism. The magnitude of this induction is considerably greater than that in dermal fibroblasts and involves up-regulation of IL-6 mRNA levels. IL-1β activates both p38 and ERK 1/2 components of the MAPK pathways. Disrupting these could attenuate the IL-6 induction. The up-regulation involves enhanced IL-6 gene promoter activity and retardation of IL-6 mRNA decay by IL-1β. Dexamethasone completely blocked the effect of IL-1β on IL-6 expression. Orbital fibroblasts also express higher levels of IL-6R than do skin-derived cells. When treated with rIL-6 (10 ng/ml), STAT3 is transiently phosphorylated. Thus, the exaggerated capacity of orbital fibroblasts to express high levels of both IL-6 and its receptor in an anatomic site-selective manner could represent an important basis for immune responses localized to the orbit in Graves’ disease.

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“…10 All assays were done in duplicate. The detection limit of the assay was 4 pg/ml and the intra-assay and inter-assay coefficients of variation were 7% and 12%, respectively.…”

Section: Cytokine Assaymentioning

confidence: 99%

“…3,8 Consequently, differences in the pattern of cytokine secretion, especially that of IL-5 and IL-12, were further studied to identify a possible role of these cytokines in the pathogenesis of AITD. [9][10][11] Thyroid autoimmunity is being increasingly identified as the underlying cause of goitre in India subsequent to the implementation of the salt iodization program in the country. 12 Meanwhile, there is a paucity of literature on the immunopathogenesis of AITD among the Indian population.…”

mentioning

confidence: 99%

The role of T-lymphocyte subsets and interleukin-5 blood levels among Indian subjects with autoimmune thyroid disease

Gopalakrishnan¹,

Sen²,

Adhikari³

et al. 2010

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OBjEcTIVE: Autoimmune Thyroid Disease (AITD) results from an interaction of exogenous and endogenous factors in a genetically predisposed individual. AITD is being increasingly reported among the Indian population. Lymphocyte subsets and levels of interleukin-5 (IL-5) were studied in the peripheral blood of patients with AITD. DESIGN: Subjects diagnosed with either hyperthyroidism due to Graves' Disease (GD) or with primary hypothyroidism due to Hashimoto's Thyroiditis (HT) were consecutively recruited. Euthyroid controls were also recruited for comparison. Lymphocyte subsets (cD4 and cD8 counts, cD4/cD8 ratio) were evaluated by flow cytometry and IL-5 levels were determined by the sandwich ELISA method. RESULTS: Nineteen subjects with GD, 16 subjects with HT and 10 controls were studied. cD4/cD8 ratios were found to be significantly lower only in subjects with HT compared to controls. Serum IL-5 values were significantly higher in both GD and HT in comparison to controls. cONcLUSIONS: The study found increased levels of IL-5 and reduction in ratios of cD4/cD8 lymphocytes in the peripheral blood of patients with HT, but only IL-5 was increased in GD. High levels of IL-5 could have resulted in the high titres of antithyroid antibodies and may therefore be considered to play a more significant role than peripheral lymphocytes in the pathogenesis of AITD in the Indian population.

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Increased Serum Concentration of Interleukin-5 in Patients with Graves' Disease and Hashimoto's Thyroiditis

Cited by 40 publications

References 15 publications

Thyroid hormone increases mannan-binding lectin levels

Thyroid hormone increases mannan-binding lectin levels

IL-1β Induces IL-6 Expression in Human Orbital Fibroblasts: Identification of an Anatomic-Site Specific Phenotypic Attribute Relevant to Thyroid-Associated Ophthalmopathy

The role of T-lymphocyte subsets and interleukin-5 blood levels among Indian subjects with autoimmune thyroid disease

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