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PubMed2006

Integrative study of hypothalamus-pituitary-thyroid-immune system interaction: thyroid hormone-mediated modulation of lymphocyte activity through the protein kinase C signaling pathway.

Thyroid hormones play critical roles in differentiation, growth and metabolism, but their participation in immune system regulation has not been completely elucidated. Modulation of in vivo thyroid status was used to carry out an integrative analysis of the role of the hypothalamus-pituitary-thyroid (HPT) axis in T and B lymphocyte activity. The participation of the protein kinase C (PKC) signaling pathway and the release of some cytokines upon antigenic stimulation were analyzed. Lymphocytes from hyperthyroid mice displayed higher T-and B-cell mitogen-induced proliferation, and those from hypothyroid mice displayed lower T- and B-cell mitogen-induced proliferation, compared with euthyroid animals. Reversion of hypothyroid state by triiodothyronine (T3) administration recovered the proliferative responses. No differences were found in lymphoid subset balance. Both total PKC content and mitogen-induced PKC translocation were higher in T and B cells from hyperthyroid mice, and lower in cells from hypothyroid mice, compared with controls. Levels of thyroid-stimulating (TSH) and TSH-releasing (TRH) hormones were not directly related to lymphocyte proliferative responses. After immunization with sheep red blood cells (SRBCs) and re-stimulation, in vitro spleen cells from hyper- or hypothyroid mice showed, respectively, increased or decreased production of interleukin (IL)-2 and interferon (IFN)-gamma cytokines. Additionally, an increase in IL-6 and IFN-gamma levels was found in hyperthyroid cells after in vivo injection and in vitro re-stimulation with lipopolysaccharide (LPS). Our results show for the first time a thyroid hormone-mediated regulation of PKC content and of cytokine production in lymphocytes; this regulation could be involved in the altered responsiveness to mitogen-induced proliferation of T and B cells. The results also confirm the important role that these hormones play in regulating lymphocyte reactivity.

Animals↗
PubMed2004

Thyroid hemiagenesis with postpartum silent thyroiditis.

A 28-year-old woman with thyroid hemiagenesis, who had been diagnosed as having Graves' disease, became pregnant during the course of methimazole treatment. The treatment was terminated in the second trimester. She delivered a normal infant at full term. She became thyrotoxic 3 months after the delivery, hypothyroid 6 months after the delivery, and finally euthyroid 11 months after the delivery without undergoing any treatment. This clinical course indicates that she developed silent thyroiditis after the delivery. A diagnosis of thyroid hemiagenesis was made on the basis of ultrasonography of the thyroid and 99mTc-pertechnetate thyroid scintiscan.

Adult↗
PubMed1995

Thyroid antibodies in association with thyroid malignancy II: Qualitative properties of thyroglobulin antibodies.

Qualitative properties of thyroglobulin (Tg) antibodies, in association with thyroid malignancy, suspected malignancy or other thyroid diseases, were studied in 177 patients. Retrospective clinical analysis revealed 137 patients to have thyroid carcinoma and 40 to have other thyroid diseases. Serum Tg was assayed by an immunoradiometric method. Thyroid microsomal (AMC) and Tg antibodies were measured by the particle agglutination method and the avidity of Tg antibodies by enzyme immunoassay (EIA). Assessment of the qualitative properties of Tg antibodies revealed that the high-avidity antibodies especially seem to bind circulating Tg. Thus any Tg value from a sample with detectable Tg antibodies is unreliable and should be interpreted with caution.

Adolescent↗
PubMed1977

Effects of thyrotropin and thyroid hormones in vivo on thyroid responsiveness to thyrotropin in vitro.

The thyroid gland of rats fed propylthiouracil is known to be unresponsive in vitro to thyrotropin; to investigate further the underlying mechanism groups of rats were variously treated with propylthiouracil and thyroid hormone or subjected to hypophysectomy. In vitro responsiveness of the thyroids was tested by measuring an increase in the concentration of c AMP when thyrotropin or prostaglandin E1 was added to the medium. Results showed that responsiveness to thyrotropin partially returned with rats fed prophylthiouracil and hypophysectomized 5, but not 2, days before death; hypophysectomy of normal rats led to increased in vitro responsiveness to thyrotropin and this was partially reversed by injections of thyrotropin for a week before death. Administration of thyroid hormone had little effect in these investigations and in vitro responsiveness to prostaglanding E1 was not consistently influenced by any of the in vivo regimens. From this experience we conclude that, at least as studied in vitro, circulating thyrotropin has a significant role in modulating responsiveness of the thyroid to thyrotropin.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1992

Antibodies in the serum of patients with autoimmune thyroid disorders react with a recombinant 98 amino acid fragment of a full length 64 kDa eye muscle membrane protein which is also expressed in the thyroid.

We have tested sera from patients with autoimmune thyroid disorders with or without ophthalmopathy for immunoreactivity, in a dot blot assay, against a recombinant 98 amino acid fragment of a cloned 64 kDa protein, D1, which is expressed in human eye muscle and thyroid, in the form of a Lac Z fusion protein. Tests were positive in 19 out of 40 patients with established thyroid-associated ophthalmopathy (TAO), in 12 out of 21 patients with Graves' hyperthyroidism (GH) without clinically evident ophthalmopathy, in 5 out of 10 patients with thyroid autoimmunity and lid retraction but no other signs of ophthalmopathy, in 4 out of 23 patients with Hashimoto's thyroiditis (HT) without evident ophthalmopathy and in 2 out of 18 patients with benign adenoma or multinodular goitre, but in only 2 out of 37 normal subjects tested. SDS-polyacrylamide gel electrophoresis and Western blotting for an antibody reactive with a 64 kDa antigen in pig eye muscle membranes was also carried out on sera from patients with TAO and GH. While immunoblotting for antibodies reactive with a 64 kDa protein was more often positive in patients with TAO, in whom 58% had serum antibodies which reacted with a 64 kDa protein, this was not the case in patients with GH without eye signs in whom the prevalence of positive immunoblot tests was 35%. Overall there was a fairly close correlation between the two tests although there were many exceptions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Immunocytochemical localisation of interleukin-1 alpha and interleukin-6 in thyroid tissues from patients with neoplastic or autoimmune thyroid disorders.

We describe the distribution of interleukin-6 and interleukin-1 alpha in thyroid tissues obtained from patients with autoimmune diseases or neoplastic thyroid disorders employing immunohistochemistry in sections from paraffin embedded tissue blocks. Interleukin-6 was found in thyroid follicular epithelial cells (TFEC) from papillary carcinomas (four of five patients) but not in follicular carcinomas (five patients). Interleukin-6 was also detected in non-toxic multinodular goiters (four of seven patients), in patients with Graves' disease who did not have an early recurrence of hyperthyroidism after surgery (three of four patients), in follicular adenomas (five of nine patients), in Hashimoto's thyroiditis (two out of six patients, both belonging to a group of three with an early stage of the disease), and in paraadenomatous tissues (in three of nine patients). Interleukin-1 alpha positive TFEC were found less frequently than interleukin-6, and only in tissues with interleukin-6 positive TFEC. Only few interleukin-6 and interleukin-1 alpha positive interstitial cells were found, even in the lymphocyte infiltrates (in both the autoimmune, benign or malignant disorders). In conclusion, both interleukin-6 and interleukin-1 alpha could be demonstrated in TFEC from patients with autoimmune diseases, benign neoplasms or papillary carcinoma, whereas follicular cancer tissues were without interleukin-6 and interleukin-1 alpha. In contrast with previous studies, interleukin-6 and interleukin-1 alpha were demonstrated in TFEC from patients with both Graves' disease and Hashimoto's thyroiditis, and the presence of these cytokines was related to the stage of the autoimmune process.

Adenoma↗
PubMed1996

Thyroid-specific T cells in the Wistar rat: 3. Induction of anergy by a syngeneic thyroid cell line.

Using a syngeneic Wistar rat model we have shown that the Wistar rat thyroid (WRT) cell line causes significant and specific proliferation of lymph node T cells from normal Wistar rats, and of splenic T cells from a thyroiditis prone line of BB/W rats, when cultured in the presence of irradiated feeder cells. These T cell responses were associated with a marked increase in the number of CD8+ T cells. However, using normal Wistar rat T cells which had been previously exposed to WRT cells, rested and then re-exposed to WRT cells as antigen, we consistently found that the T cell population had been rendered unreactive, or anergic, to further thyroid cell stimulation. However, if recombinant rat IL-2 was added to the cultures, then T cell responsivity was seen on re-exposure to WRT cells. The lymphopenic BB/W rat also had T cells which showed a primary T cell response to the WRT cell line accompanied by a marked increase in CD8+ T cells. In contrast to the Wistar rat T cells, the BB/W T cells retained a proliferative responsiveness to WRT cells on re-exposure although such responsiveness could also be markedly enhanced with IL-2. These data suggested that antigen-mediated inhibitory signals were induced in normal Wistar rat T cells by the syngeneic WRT cell line, independent of the presence of co-stimulatory molecules. Furthermore, the thyroiditis prone BB/W rat T cells appeared to be less responsive to such anergy induction, perhaps contributing to their susceptibility to autoimmune thyroid disease.

Animals↗
PubMed1983

Autoimmune granulomatous thyroiditis in inbred mice: resemblance to subacute (de Quervain's) thyroiditis in man.

Mice in various inbred strains were immunized with mouse thyroglobulin emulsified in Freund's complete adjuvant. Granulomatous thyroid lesions were observed only in RF and SJL mice. These lesions were studied ultrastructurally and showed similarities with subacute (de Quervain's) thyroiditis in man. Thyroid function tests, e.g., the concentration of serum thyroxine and thyroid radioiodine uptake showed similarities between these two diseases. Such findings have not been previously described in experimental thyroiditis.

Animals↗
PubMed2000

Transgenic expression of Fas ligand on thyroid follicular cells prevents autoimmune thyroiditis.

"Immune privilege" is defined as tissue resistance to aggression by specifically activated lymphocytes, and involves the interaction between Fas expressed on infiltrating cells and Fas ligand (FasL) constitutively expressed on the target tissue. To test whether ectopic expression of FasL on thyrocytes could prevent autoimmune aggression of the thyroid by activated lymphoid cells, three lines of transgenic mice expressing low, intermediate, and high levels of functional FasL on thyroid follicular cells were generated. Experimental autoimmune thyroiditis was induced by immunization with mouse thyroglobulin. In all of the experiments, the effects were dependent on the level of FasL expression. Low and intermediate expression had no or only weak preventive effects, respectively, whereas high FasL expression strongly inhibited lymphocytic infiltration of the thyroid. Anti-mouse thyroglobulin-proliferative and cytotoxic T cell responses, as well as autoantibody production, were diminished in transgenic mice expressing high levels of FasL relative to controls. Furthermore, in these latter mice Th1 responses to mouse thyroglobulin were profoundly down-regulated, uncovering a new potential role for FasL in peripheral tolerance to organ-specific Ags. In sum, the prevention of experimental autoimmune thyroiditis by FasL on thyrocytes is dependent on the level of FasL expression.

Animals↗
PubMed2006

Monoclonal pathogenic antibodies to the thyroid-stimulating hormone receptor in Graves' disease with potent thyroid-stimulating activity but differential blocking activity activate multiple signaling pathways.

The thyroid target Ag for disease-inducing autoantibodies in Graves' disease is the receptor for thyroid-stimulating hormone (TSH), but little is known about the molecular basis of this pathogenic Ab response. We describe the characteristics of two high- affinity mAbs developed from an experimental murine model of hyperthyroid Graves' disease that exhibit potent thyroid-stimulating activity. Nanogram concentrations of the IgG mAbs KSAb1 and KSAb2 and their Fab induce full stimulation of the TSH receptor that is matched by the ligand TSH and, thus, act as full agonists for the receptor. However, KSAb1 and KSAb2 display differential activities in their ability to block TSH-mediated stimulation of the receptor, indicating subtle differences in their biological properties. In displacement studies, IgG and Fabs of KSAb1 and KSAb2 compete with Graves' disease autoantibodies as well as thyroid-blocking Abs present in some hypothyroid patients, indicating a close relationship between these autoimmune determinants on the receptor. In passive transfer studies, single injections of microgram quantities of KSAb1 or KSAb2 IgG led to rapid elevation of serum thyroxine and a hyperthyroid state that was maintained for a number of days. The thyroid glands showed evidence of cell necrosis, but there was no accompanying mononuclear cell infiltrate. In studying their receptor activation pathways, both KSAb1 and KSAb2 provoked phosphorylation of the intracellular ERK1/2 pathway in primary thyrocytes, indicating that multiple signaling pathways may participate in the pathogenesis of Graves' disease. In summary, our findings emphasize the similarities of the experimental mouse model in reproducing the human disorder and provide improved means for characterizing the molecular basis of this pathogenic response.

Animals↗
PubMed1999

Thyroid testing and thyroid hormone replacement in patients with sleep disordered breathing.

The current literature recommends that patients who have symptoms of sleep disordered breathing should be evaluated for hypothyroidism. Thyroid hormone replacement therapy has been reported by some authors to be effective in treating obstructive sleep apnea in hypothyroid patients. The present study prospectively evaluated the prevalence of hypothyroidism in 1,000 consecutively presenting patients who came to the office for evaluation of snoring or obstructive sleep apnea syndrome. The authors also examined the efficacy of treatment for hypothyroidism on sleep apnea in patients with both disorders. Of the 1,000 patients, routine thyroid testing was performed on 834; only 10 of these patients (1.2%) were discovered to have previously undiagnosed clinical hypothyroidism. Four of the 10 patients with newly diagnosed clinical hypothyroidism had obstructive sleep apnea syndrome, and they received thyroid hormone replacement therapy. Once these four patients achieved a euthyroid state, repeat polysomnography showed that there was no significant difference between their pre- and posttreatment respiratory disturbance index. Based on the results of our study, we conclude the following: 1) The prevalence of hypothyroidism in patients who are evaluated for sleep disordered breathing is no greater than that of the general population. 2) Thyroid replacement therapy results in little or no improvement in sleep apnea in patients with clinical hypothyroidism. 3) Routine thyroid function screening is not indicated for patients who are being evaluated for sleep disordered breathing.

Adult↗
PubMed1999

[A case of primary thyroid lymphoma with Hashimoto thyroiditis].

A seventy four year old man presented with a mass of the thyroid which was diagnosed as a lymphoma arising from the thyroid gland with Hashimoto thyroiditis. Postoperative course was complicated by the tumor reoccurence presenting as invasion of the larynx with a critical narrowing of the lumen of the larynx. With chemotherapy complete remission has been achieved. This case illustrates common aetiology of the thyroid lymphoma of MALT type and Hashimoto thyroiditis.

Aged↗
PubMed1992

Gi alpha-1 expression in the human thyroid is regulated by TSH: loss of regulation in thyroid autonomous adenoma.

The molecular mechanisms underlying the development of endocrine active thyroid tumors are poorly understood. These tumors produce excess thyroid hormone, which then suppresses TSH (thyroid stimulating hormone) production. In the present report, we show that the expression of Gi alpha-1 is under control of TSH in the normal human thyroid. In contrast Gi alpha-1 escapes TSH control in autonomous adenoma and thus is constitutively expressed. Since receptor-mediated activation of Gi controlled pathways is known to elicit a proliferative response in several cell types, we propose that in thyroid adenomas the unregulated constitutive expression of Gi alpha-1 is causally related to the autonomous growth.

Adenoma↗
PubMed2002

Quantitative indicators of sonographic image of thyroid gland and their relation to antithyroid antibodies in Hashimoto's lymphocytic thyroiditis.

Sonography is a widely used non-invasive diagnostic tool and its main advantage is low cost in comparison with other diagnostic methods such as immunological analyses. In this work it is presented the relation between a sonographic image of thyroid gland and an immunological status of the patients with Hashimoto's lymphocytic thyroiditis (chronic inflammation of the thyroid gland). The results, evaluated on a set of 740 B-mode sonographic images from 37 subjects, show that raw values of individual image pixels in sonogram of thyroid gland with presence and without presence of anti-thyroid antibodies are significantly different (means 31.87 and 44.56; standard deviations 8.6 and 11.82; t = 3.4; p = 0.0017) and that they can be used for the prediction of presence of anti-thyreoglobulin and anti-thyreoperoxidasis antibodies. This result suggests the possibility to use this method in clinical diagnostic process for reducing the costs. Also the correlation between the image features and the level of antibodies was examined. The highest correlation was found for inverse difference moment and the level of anti-thyreoperoxidasis (coefficient of determination 0.43).

Autoantibodies↗
PubMedDate not supplied

[Incidental thyroid microcarcinoma in benign thyroid disease. Incidence in a total of 100 consecutive thyroidectomies].

Over the past few years, incidental thyroid microcarcinoma has become a frequent disease and its incidence in some reports is considerable. Discovering new cases depends on the extended indications for total thyroidectomy for benign disease, on progress in the field of diagnostic instruments (ultrasound, scintigram, fine needle biopsy for cytology, CT scan, MRI), and on the pathology examination of very thin slices of specimens. In spite of the high incidence reported in some autopsy series, suggesting that this tumour may have a good prognosis, some Authors report an overall incidence of up to 11% of local recurrence, metastasis or mortality. For all these reasons the surgical treatment of incidental thyroid microcarcinoma is still controversial. The aim of this study was to estimate the incidence and examine the clinical-pathological findings of incidental thyroid microcarcinoma in a series of 100 consecutive thyroidectomies and to evaluate whether complete removal of the gland should be adopted in all cases. In the present series the incidence of incidental thyroid microcarcinoma was 21.6% (19/88). Total thyroidectomy was considered the treatment of choice for diffuse benign disease and appeared to be necessary for both the diagnosis and treatment of incidental thyroid microcarcinoma.

Adult↗
PubMed1975

Diminished binding of thyroid-stimulating hormone in a transplantable rat thyroid tumor as a possible cause of hormone unresponsiveness.

The adenylate cyclase activity and the binding of 125I-labeled thyroid-stimulating hormone (TSH) of normal and tumor rat thyroid plasma membranes were compared. No significant difference in the basal and fluoride-sensitive adenylate cyclase activity between normal and tumor plasma membranes was observed. Thyroid plasma membranes responded to TSH, whereas the enzyme from the tumor plasma membranes was TSH insensitive. Thyroid plasma membranes boud 125I-TSH. Tumor plasma membranes bound 125I-TSH poorly. At the highest concentration of unlabeled TSH used, 80% of the 125I-TSH that was bound to thyroid plasma membranes was displaced, whereas only 10% of the 125I-TSH bound to tumor plasma membranes was displaced. Therefore, it seems likely that the failure of this tumor to respond to TSH is due to an alteration in the functional unit of membrane adenylate cyclase at the level of the receptor subunit.

Adenylyl Cyclases↗
PubMed1990

[Clinical epidemiology of autoimmune thyroid disorders--variation of natural history in patients with autoimmune thyroid disorders].

Clinical and epidemiological study for autoimmune thyroid disorders was performed in a rural community. Ninety-six of 1,686 subjects had asymptomatic autoimmune thyroiditis and were followed from 1979 to 1988. TRH loading test was carried out in 91 of 96 cases between 1983 and 1984. Each individual was classified into 4 subgroups. Five patients had normal levels of basal plasma TSH and had no increment of peak levels of plasma TSH (Grade G). Twenty-three had normal levels of both basal and peak plasma TSH (Grade I). The peak plasma TSH levels in 53 patients was high, but the basal was within the normal range (Grade II). Ten had high levels of both basal and peak plasma TSH (Grade III). One of the 5 Grade G cases developed overt Graves' disease in 1987 and another Grade III case suffered from goitrous Hashimoto's thyroiditis with primary hypothyroidism. Four of the ten Grade III cases and one Grade II case developed primary myxedema during the observation period. These results show that the natural history of asymptomatic autoimmune thyroiditis is variable and the prevention of overt autoimmune thyroid disorders is difficult.

Aged↗
PubMedDate not supplied

[Thyroid function in persons with hyperplasia of the thyroid gland in the presence of iodine deficiency].

The levels of thyroxine (T4), triiodothyronine (T3), reverse triiodothyronine (RT3), thyroxine-binding capacity (TBC), a free thyroxine index (FT4I) and thyroid-stimulating hormone (TSH) were studied by a radioimmunoassay in the blood of healthy schoolchildren aged 14 to 17 with stage I-II of thyroid hyperplasia residing in a mountain region of the Transcarpathian area, the Ukrainian SSR, with noticeable environmental iodine deficiency. Similar studies were conducted in a lowland region with a sufficient iodine level. A decrease in the concentration of T4, T3, RT3 and FT4I and higher TBC and TSH values were established in the healthy schoolchildren from the mountain region as compared to corresponding values in the schoolchildren from the lowland region indicating a lower level of homeostasis of thyroid hormones in the mountain region. A decrease in indices of thyroid function was observed in hyperplasia as compared to indices of the healthy, schoolchildren (T3 and TSH levels were higher) both in the mountain and lowland regions. More pronounced shifts were revealed in the blood of the schoolchildren from the mountain region. Less iodine was excreted with daily urine in the healthy schoolchildren from the mountain region than in the schoolchildren from the lowland region. Schoolchildren with hyperplasia excreted less iodine than healthy children, iodine excretion being lower in the schoolchildren from the mountain region. The results obtained suggested the hypothyroid nature of thyroid hyperplasia in the mountain region. The importance of iodine prophylaxis was emphasized.

Adolescent↗