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PubMed1989

[Autoantigens in autoimmune thyroid diseases].

Human thyroid peroxidase (TPO) was found to bind with both IgG and IgM from patients with autoimmune thyroid diseases. Furthermore, binding of IgG to microsomes was inhibited by TPO. Patients' IgG that passed through an antigen column packed with TPO-coupled Sepharose 4 B beads lost their hemagglutinating activity in microsome hemagglutination test. Various strains of mice were immunized with porcine TPO emulsified in complete Freund's adjuvant. Both C 57 BL/6 and C 57 BL/10 mice showed mononuclear cell infiltration in the thyroid with very high incidences of thyroiditis. The strains of mice showing thyroiditis were very different from high responder strains that were immunized with murine thyroglobulin. Cloning of human TPO cDNA was attempted to deduce the primary structure of human TPO. Using three kinds of oligonucleotides as probes, two cDNAs, 2.8 and 2.4 kb, were selected from a cDNA library constructed from mRNA purified from Graves' disease thyroid. Sequencing of cDNAs revealed that shorter cDNA lacked 171 nucleotides at the middle portion of the longer cDNA. Primer extension analysis of mRNA indicated that the full length cDNA of human TPO consists of 3,048 nucleotides and its open reading frame codes 933 amino acids.

Animals↗
PubMed1998

Linkage analysis of candidate genes in autoimmune thyroid disease. III. Detailed analysis of chromosome 14 localizes Graves' disease-1 (GD-1) close to multinodular goiter-1 (MNG-1). International Consortium for the Genetics of Autoimmune Thyroid Disease.

The autoimmune thyroid diseases [Graves' and Hashimoto's diseases (GD and HT)] develop in genetically susceptible individuals, but the genes responsible for this susceptibility remain unknown. To identify such genes, we have been testing candidate genes and chromosomal regions using highly polymorphic microsatellite markers. We recently reported evidence for the first locus linked to GD (GD-1) on chromosome 14q31 in a small group of families. We have now extended these studies and analyzed 53 multiplex families with GD and/or HT (323 individuals). Chromosome 14 was screened using 16 microsatellite markers spanning the entire chromosome. Three additional markers located inside candidate genes on chromosome 14 were also studied. Microsatellite markers were amplified using fluorescent-labeled primers and separated on an ABI-310 genetic analyzer. The data were analyzed using LIPED software for two-point logarithm of odds (LOD) score analysis and GeneHunter software for multipoint linkage analysis. No linkage of any marker was found to HT or autoimmune thyroid diseases (GD+HT). The previously identified GD-1 locus on 14q31 continued to show evidence of linkage to GD in this much larger set of families. The maximum LOD score was 2.1 obtained for marker D14S81 (theta=0.01), assuming a recessive mode of inheritance and a penetrance of 0.3. Multipoint analysis yielded a maximum LOD score of 2.5 between markers D14S81 and D14S1054. There was no evidence for heterogeneity in our sample. These data again suggest the presence of a major Graves' disease susceptibilitygene (GD-1) on chromosome 14q31. This locus is close to the recently identified multinodular goiter-1 locus.

Autoimmune Diseases↗
PubMed2002

Disease associations with autoimmune thyroid disease.

Autoimmune thyroid disease (AITD) is common and occurs frequently in conjunction with other diseases. Many putative disease associations have been suggested for AITD but the validity of these associations is not clear in all cases. It is important to define disease associations correctly because this may offer a means to rationally screen for true associations, may shed light on shared pathophysiologic mechanisms and may be important if the associated disease impacts on patient management. This review has examined the evidence base for a large number of the suggested associations.

Digestive System Diseases↗
PubMed1999

[B-cell, T-cell surface phenotypes and epitopes in autoimmune thyroid diseases].

Autoimmune thyroid diseases (AITD) are categorized as organ specific autoimmune diseases, including Graves' disease (GD), Hashimoto's thyroiditis and idiopathic myxoedema. In this article, B-, T-cell surface phenotypes and epitopes in AITD were reviewed. It has been reported that the proportion and absolute number of B and T lymphocyte subpopulation or CD4/8 ratio in peripheral blood from AITD was not different from normal subjects. Those of CD5+ B cells and gamma delta T cells known as autoreactive clones were, however, increased in peripheral blood from GD. In the thyroid tissue of AITD, B-cells with activated markers were predominantly infiltrated rather than T-cells. The CD4/8 ratio and the proportion of CD8+CD11b+ T (suppressor T) cells was decreased in contrast to the increase of CD8+CD11b- T (cytotoxic T) cells. The CD4+4B4+ T (helper/inducer) cells were more predominant than CD4+2H4+ T (suppressor/inducer) cells in thyroid tissue from GD. These abnormality might cause the cell destruction and the enhanced autoantibody production in the tissue of AITD. Thyroglobulin, thyroid peroxidase and thyroid stimulating hormone receptor are known as major autoantigens in AITD. Recently, B-cell and T-cell epitopes on these autoantigen molecules have been defined, using monoclonal antibodies, proteolytic or synthetic peptides with molecular gene engineering. These epitope analysis would be contributed to the autoimmune tolerance in AITD.

Autoimmune Diseases↗
PubMed1984

Relationship of thyroid disease and use of thyroid supplements to breast cancer risk.

An interview study of 1362 breast cancer cases and 1250 controls identified through a multi-center screening program allowed evaluation of effects of thyroid disease and supplementation on breast cancer risk. A previous diagnosis of treated thyroid disease was not associated with an excess risk (RR = 1.0), nor were any specific diagnoses, including hypothyroidism, hyperthyroidism, or goiter. Although based on limited numbers, women with untreated hypothyroidism or goiter had a significantly reduced risk of breast cancer (RR = 0.3, 95% CI 0.1-0.7). Thyroid supplementation for non-disease reasons (primarily weight loss and fertility problems) was associated with a slight elevation in breast cancer risk (RR = 1.2, 95% CI 0.9-1.7), but patterns of risk by duration and latency generally failed to provide evidence of causality. Elevated risks were noted among women who received thyroid medications for fertility problems (RR = 4.2) and among those with a family history of breast cancer (RR = 2.6) or a late age at first childbirth (RR = 2.4), possibly indicating an hormonal interaction.

Adult↗
PubMed2003

CTLA-4 and its role in autoimmune thyroid disease.

Autoimmune thyroid disease (AITD) occurs in two common forms: Graves' disease and Hashimoto thyroiditis. On the basis of functional and experimental data, it has been suggested that the gene encoding cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) is a candidate gene for conferring susceptibility to thyroid autoimmunity. In this review, we critically evaluate the evidence for pathogenetic involvement of CTLA-4 in the various forms of AITD and focus on the possible role of genetic variation of the CTLA4 locus. Population genetics data strongly suggest a role for the CTLA4 region in susceptibility to AITD. However, further functional studies are required to understand the significance of CTLA4 polymorphisms in the pathogenic mechanism of AITD.

Antigens, CD↗
PubMed2005

[Multifactorial analysis of effects of mothers' autoimmune thyroid disease on their infants' intellectual development].

OBJECTIVE: To analyze factors relevant to retarded intellectual development in infants born to mothers with autoimmune disease of thyroid. METHODS: All the term newborns born to mothers with autoimmune thyroid disease (selection criteria) without asphyxia in all county, city, and provincial hospitals in Zhejiang province (except for Ningbo City) from July 2001 to June 2003 were enrolled through Zhejiang provincial neonatal disease screening network system. The control group was consisted of the neonates who were born to mothers without thyroid disease in these hospitals during the same period. Heel capillary blood samples were collected from the neonates older than 3 days in local hospitals and sent to the center of Zhejiang provincial neonatal disease screening network system. TSH levels were measured by Time Difference Fluorescent Analysis Device (1420 II type, EGG Company, US). If the level of TSH was higher than 9 mU/L, their mothers were called back to the center with their infants within 3 days. If the level of TSH was normal, they were called back to hospitals at age of 28 - 35 days of infants. The pattern of maternal thyroid disease, duration, thyroid function, the history of maternal drug administration, maternal age, gestational age and body weight of the neonates were recorded. The neonatal and maternal serum thyroid function tests were re-performed and the serum TPOAb, TGAb, TRAb and TSAb levels in both neonates and their mothers were measured as well. A 1-year follow-up study was done and all these subjects were investigated by means of Gesell development schedules by special investigators at the age of 1, 3, 6 and 12 months. The results were expressed as developmental quotient. Case-sectional study was performed. Statistical analyses were conducted using SPSS software. The multiple logistic regression analysis was used to analyze factors which might have effect on infantile personal-social ability, adaptive ability, gross motor ability or the fine-motor ability. One-way ANOVA was used to compare those five subfields ability followed by LSD multiple comparisons and Dunnet's C test was used when variances were not equal. Correlation analysis was used to compare the anti-thyroid antibody between neonates and their mothers. RESULTS: Poor personal-social ability, adaptive ability, gross motor ability and fine motor ability of infants born to mothers with autoimmune thyroid diseases were found as compared to the infants born to healthy mothers (P < 0.01). Moreover, the infants born to mothers with Hashimoto's thyroiditis had significantly poorer fine motor ability and adaptive ability than those born to mothers with Grave's disease (P < 0.05). The Spearman correlation coefficients of TPOAb, TGAb, TRAb and TSAb were 0.636, 0.574, 0.619 and 0.473, respectively, and all the P values were lower than 0.01.The multifactor logistic regression analysis showed that infantile TPOAb levels and maternal TRAb levels were associated with infantile personal-social ability, adaptive ability, and gross motor; while maternal TPOAb levels and thyroid function during gestation were associated with infantile fine-motor ability (P < 0.05). CONCLUSION: Maternal autoimmune thyroid diseases during pregnancy had adverse effects on intellectual development of infants. The maternal levels of TPOAb, TRAb and thyroid status were associated with the infantile personal-social ability, adaptive ability, gross motor and fine motor development. In order to reduce the effect on infant, it is necessary to treat adequately the maternal autoimmune thyroid diseases during pregnancy.

Adult↗
PubMed2004

Ultrastructural localization of thyroid peroxidase, hydrogen peroxide-generating sites, and monoamine oxidase in benign and malignant thyroid diseases.

Despite thyroid tissue heterogeneity, biochemical and morphological features have been associated with certain thyroid diseases. We analyzed the ultracytochemical localization of thyroperoxidase (TPO), TPO-associated hydrogen peroxide-generating sites (H(2)O(2) sites), and monoamine oxidase (MAO) in terms of morphology and biochemical TPO activity in abnormal thyroids. We examined 11 cases of nontoxic multinodular goiter, 5 cases of Hashimoto's thyroiditis, 1 case of oncocytic (Hürthle or oxyphilic cell) adenoma, 5 cases of Graves' disease, 4 cases of papillary carcinoma, and 4 cases of perinodular normal tissue. In the perinodular tissue, TPO was detected mainly in the nuclear envelope, rough endoplasmic reticulum (RER), and subapical vesicles, but not in the apical surface. In multinodular goiter, heterogeneous TPO reactivity ranging from almost null to strongly positive was detected in similar locations as in the perinodular tissue, and was absent in the microvilli. Follicular cells from Hashimoto's thyroiditis displayed TPO in the nuclear envelope and the scarce RER. Remarkably, oncocytic cells from both Hashimoto's thyroiditis and oncocytic adenoma, typically packed with mitochondria, displayed evident TPO reaction exclusively in mitochondrial cristae. In Graves' disease, the nuclear envelope, enlarged RER, and apical vesicles were strongly TPO positive, and microvilli also exhibited TPO activity. Papillary carcinoma cells were negative for TPO. The localization and characteristics of TPO activity in the H(2)O(2) sites were similar to that of TPO in all tissues. MAO was positive in mitochondria of perinodular tissues, multinodular goiter, and oncocytes and negative in Hashimoto's thyroiditis and Graves' disease. Interestingly, MAO was intensely positive in the nuclear envelope of papillary carcinoma but unreactive in mitochondria. Biochemical TPO activity was increased in multinodular goiter and Graves' disease. In conclusion, several changes in ultracytochemical characteristics of TPO, H(2)O(2) sites, and MAO were associated with thyroid disease. Nonmalignant oncocytic cells exhibited an unusual mitochondrial location of TPO and H(2)O(2) sites. The distribution of MAO in nuclear envelope of papillary carcinoma cells could be a further feature of malignancy.

Humans↗
PubMed1985

Purification of the human thyroid peroxidase and its identification as the microsomal antigen involved in autoimmune thyroid diseases.

Human thyroid peroxidase (TPO) has been purified from thyroid microsomes by immunoaffinity chromatography using a monoclonal antibody (mAb) to TPO. The eluted material had a specific activity of 381 U/mg and exhibited a peak in the Soret region. The ratio of A411 to A280 ranged from 0.20 to 0.25. Upon SDS-polyacrylamide gel electrophoresis, the purified enzyme gave two contiguous bands in the 100 kDa region. Further, it has been demonstrated that sera with anti-microsomal autoantibodies from patients presenting Graves' or Hashimoto's thyroiditis diseases were able to bind to purified TPO and to inhibit in a dose-dependent manner the mAb binding to purified TPO. This suggests that TPO is the thyroid antigen termed to date the microsomal antigen.

Antibodies, Monoclonal↗
PubMed2006

[Susceptibility genes for the development of autoimmune thyroid disease].

Autoimmune thyroid disease (AITD) is caused by an immune response to self thyroid antigens. Twin studies and familial aggregation indicated that AITD is a complex disease with genetic factors and major histocompatibility complex is the most clearly established genetic factor. We confirmed the association of the co-receptor CTLA4 with AITD. We have identified the association of the SNP in the Fc receptor-like 3 with several autoimmune diseases, including AITD, SLE and rheumatoid arthritis, which SNP affected the level of autoantibody production. Furthermore, we have identified ZFAT as a susceptibility gene in 8q24 for AITD by whole-genome linkage analysis and further SNP-based dense mapping. The associated SNP in ZFAT affected the antisense transcript of ZFAT, which in turn affected the ZFAT expression.

Antigens, CD↗
PubMed1995

Cellular immunity in autoimmune thyroid disease.

Autoimmune thyroid disease occurs in a genetically susceptible patient after triggering events including bacterial and viral infections, environmental insults, drugs or hormones. These triggering events may break the tolerance to self-antigen, leading to emergence of autoreactive T cells. One or more T cell clones that recognize the self-antigen is(are) assumed to be involved in initiating autoimmune processes. Following this, T cell clones expand and migrate from the peripheral blood into the thyroid gland. Migration of mononuclear cells is controlled by inflammatory cytokines and adhesion molecules. Intrathyroidal T cells may interact with dendritic-like cells, thyrocytes expressed with HLA-DR antigens, B cells and extracellular matrix, resulting in the proliferation of T cells, production of cytokines and autoantibodies. These interactions are also regulated by inflammatory cytokines and adhesion molecules. When the initial immune response is completed, a secondary immune response ensues, that may be of considerable complexity involving reaction of infiltrating T cells to a variety of tissue-specific and tissue-non-specific antigens. These immune responses may contribute to the recurring immunologic activity and maintenance of autoantibody overproduction.

Animals↗
PubMedDate not supplied

Screening for celiac disease in patients with autoimmune thyroid disease: from research studies to daily clinical practice.

Screening procedures performed in research-setting studies have shown that the prevalence of celiac disease in patients with autoimmune thyroid disease is approximately 4-15 times higher than the general population, thus suggesting that patients with autoimmune thyroid disease should be routinely screened for celiac disease. However, the performance of these screening programs has never been evaluated in everyday, clinical-practice setting. We invited newly diagnosed patients with autoimmune thyroid disease, seen at our Hospital, to participate in a serological screening for celiac disease. Two-hundred and thirty-one patients, female to male ratio 8.89:1, mean age 41.3 +/- 18.1 years, range 7.1-80.5 years were included. The number of diagnosed celiac disease was 0. Our results do not support the usefulness of a screening for celiac disease in patients with autoimmune thyroid disease in daily practice, despite the favorable results obtained in research-setting studies. Since screening is a resource-consuming activity, for both patients and clinicians, we suggest that a careful evaluation of the yield of a screening is always warranted before its adoption in the clinical practice.

Adolescent↗
PubMed1998

Linkage analysis of candidate genes in autoimmune thyroid disease: 1. Selected immunoregulatory genes. International Consortium for the Genetics of Autoimmune Thyroid Disease.

Graves' and Hashimoto's diseases are autoimmune thyroid diseases in which the genetic contribution is complex. For this reason, identification of necessary susceptibility genes has been difficult. However, a number of immunoregulatory genes have been implicated by association studies, including: CTLA-4, a recently described protein involved in antigen presentation, located on chromosome 2q33; the T-cell receptor V alpha and V beta gene complexes, located on 14q11 and 7q35, respectively; and the Ig gene complex (IgH), located on 15q11. We used polymorphic microsatellite markers located within these genes, or gene complexes, to test for linkage (rather than association), to each of these candidates. Using markers within the loci allowed us to assume a fixed recombination fraction of 0.01 in the tested model. Three hundred eight subjects from 48 multiplex families were studied, with 142 affected subjects. Using this set of families, we have previously shown evidence of linkage with a major susceptibility locus for Graves' disease (GD-1) on 14q24.3-31, with a maximum lod (logarithm + odds) score of 2.1, at a penetrance of 80% and with a dominant mode of inheritance. In the present study, we obtained consistently negative lod scores for each of the candidate genes, assuming either dominant or recessive modes of inheritance. These data, therefore, showed evidence against linkage with all the candidate genes. Unlike association studies, linkage analyses detect major genetic influences on disease susceptibility exerted by the linked loci. The lack of linkage for the immunoregulatory genes that were studied indicated, therefore, that they were not major contributors to disease etiology.

Abatacept↗
PubMed1999

[Immunoregulatory genes in autoimmune thyroid disease].

Autoimmune thyroid diseases (AITD) has a strong genetic basis. Although several candidate genes have been studied, the AITD causing genes are still unknown. Major candidate immune regulatory genes include human leukocyte antigen (HLA) gene, Ig heavy chain genes, T cell receptor genes, IL-1 receptor antagonist gene, IL-1 alpha gene and cytotoxic T lymphocyte antigen-4 (CTLA-4) gene. The relation between HLA and AITD has extensively been studied. In addition, polymorphism of the 3'-untranslated region and codon 17 of the CTLA-4 gene has been reported to associate positively with AITD. However, no linkage analyses have showed positive relation between AITD and these candidate genes except for HLA.

Abatacept↗