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Leonidas H. Duntas - One of the best experts on this subject based on the ideXlab platform.
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The catalytic role of iodine excess in loss of homeostasis in Autoimmune Thyroiditis
Current Opinion in Endocrinology Diabetes and Obesity, 2018Co-Authors: Leonidas H. DuntasAbstract:To review the latest developments concerning the role of iodine in the pathophysiology of Autoimmune Thyroiditis. Recent studies have provided evidence that in areas with excess iodine intake, increased incidence of Autoimmune Thyroiditis marked by high titers of thyroid peroxidase and thyroglobulin antibodies has occurred. Investigations in the NOD.H2h4 mouse, a strain prone to AIT, showed that they are better adapted to the Wolff-Chaikoff effect. To provide an overview of the studies conducted during the last few years implicating iodine in the development and manifestation of Autoimmune Thyroiditis.
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The catalytic role of iodine excess in loss of homeostasis in Autoimmune Thyroiditis.
Current opinion in endocrinology diabetes and obesity, 2018Co-Authors: Leonidas H. DuntasAbstract:PURPOSE OF REVIEW To review the latest developments concerning the role of iodine in the pathophysiology of Autoimmune Thyroiditis. RECENT FINDINGS Recent studies have provided evidence that in areas with excess iodine intake, increased incidence of Autoimmune Thyroiditis marked by high titers of thyroid peroxidase and thyroglobulin antibodies has occurred. Investigations in the NOD.H2h4 mouse, a strain prone to AIT, showed that they are better adapted to the Wolff-Chaikoff effect. SUMMARY To provide an overview of the studies conducted during the last few years implicating iodine in the development and manifestation of Autoimmune Thyroiditis.
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Environmental factors and Autoimmune Thyroiditis.
Nature clinical practice. Endocrinology & metabolism, 2008Co-Authors: Leonidas H. DuntasAbstract:Autoimmune Thyroiditis, of which Hashimoto Thyroiditis represents the most frequent form, is an inflammatory state of the thyroid gland that results from the interaction between genetic variants that promote susceptibility and environmental factors. High iodine intake, selenium deficiency, pollutants such as tobacco smoke, infectious diseases such as chronic hepatitis C, and certain drugs are implicated in the development of Autoimmune Thyroiditis, primarily in genetically predisposed people. Long-term iodine exposure leads to increased iodination of thyroglobulin, which increases its antigenicity and initiates the Autoimmune process in genetically susceptible individuals. Selenium deficiency decreases the activity of selenoproteins, including glutathione peroxidases, which can lead to raised concentrations of hydrogen peroxide and thus promote inflammation and disease. Such environmental pollutants as smoke, polychlorinated biphenyls, solvents and metals have been implicated in the Autoimmune process and inflammation. Environmental factors have not yet, however, been sufficiently investigated to clarify their roles in pathogenesis, and there is a need to assess their effects on development of the Autoimmune process and the mechanisms of their interactions with susceptibility genes.
Noel R. Rose - One of the best experts on this subject based on the ideXlab platform.
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Invariant NKT Cell Lines Derived from the NOD·H2h4 Mouse Enhance Autoimmune Thyroiditis
Journal of thyroid research, 2011Co-Authors: Rajni Sharma, Patrizio Caturegli, Noel R. Rose, Xiaoguang Fan, C. Lynne BurekAbstract:To study the role of invariant Natural Killer T cell ( iNKT) cells in Autoimmune Thyroiditis, we derived two iNKT cell lines from the spleens of NOD· H2h4 mice, a strain that develops spontaneous Autoimmune Thyroiditis exacerbated by excess dietary iodine. The two lines were CD1d-restricted and expressed CD4+, DX5+, and the Vα4Jα281 gene segment, of the T-cell receptor α locus. Upon stimulation with α-galactosyl-ceramide (α-GalCer), both lines rapidly produced IL-2, IL-4, IFN-γ, IL-10, and TNF-α. Strikingly, a similar cytokine response was also induced by thyroglobulin, one of the most abundant protein in the thyroid gland and a major autoantigen in human Autoimmune Thyroiditis. Transfer of the iNKT cell lines to syngeneic hosts enhanced Autoimmune Thyroiditis. Intraperitoneal injections of α-GalCer in iodine primed mice also induced thyroid disease. This paper reports for the first time that iNKT cells respond to thyroglobulin and enhance Autoimmune Thyroiditis in iodine fed NOD·H2h4 mice.
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Autoimmune Thyroiditis and ROS
Autoimmunity Reviews, 2008Co-Authors: C. Lynne Burek, Noel R. RoseAbstract:Abstract Autoimmune Thyroiditis, also known as chronic lymphocytic or Hashimoto's Thyroiditis, is characterized by infiltration of the thyroid gland by inflammatory cells and production of autoantibodies to thyroid-specific antigens thyroglobulin and thyroperoxidase. It is accompanied by hypothyroidism due to destruction and eventual fibrous replacement of the follicle cells. Autoimmune Thyroiditis is clearly multifactorial in etiology with genetic and environmental factors contributions. Excess dietary Iodine can exacerbate Thyroiditis in genetically susceptible hosts such as the NOD.H2 h4 mouse. In this mouse excess dietary iodine leads to an increased immunogenicity of the thyroglobulin molecule and enhanced expression of ICAM-1 on thyroidal follicle cells. We present evidence here that ICAM-1 expression is enhanced by the elevated generation of reactive oxygen species (ROS). The anti-oxidant diphenyleneiodium (DPI), an inhibitor of NADPH oxidase, reduced both the generation of ROS and of ICAM-1 expression in cultures of NOD.H2 h4 mouse thyrocytes. These results suggest that antioxidants may have therapeutic value in preventing Autoimmune Thyroiditis.
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Linking lodine with Autoimmune Thyroiditis
Environmental Health Perspectives, 1999Co-Authors: Noel R. Rose, Linda Rasooly, Ali M. Saboori, C. Lynne BurekAbstract:A great deal of circumstantial evidence has linked iodine with the rising incidence of Autoimmune Thyroiditis in the United States. In our investigations, we have shown directly that T cells from humans with chronic lymphocytic Thyroiditis proliferate in the presence of iodinated but not in the presence of noniodinated human thyroglobulin. Moreover, the proliferative response is restored when the thyroglobulin is iodinated artificially in vitro. Using a panel of monoclonal antibodies, we found evidence that the presence of iodine induces a number of stereochemical changes in the conformation of the molecule, resulting in the loss of some antigenic determinants and the appearance of others. One prominent determinant was associated with the iodine-containing amino acid thyroxine. Both the number and position of the iodine substituents determine the precise specificity of this epitope. A new model for the study of the role of iodine in inducing thyroid autoimmunity has become available in the form of the nonobese diabetic (NOD)-H2(h4) mouse. This animal develops Autoimmune Thyroiditis spontaneously but in relatively low prevalence. However, if iodine is added to the drinking water, the prevalence and severity of the thyroid lesions increase markedly. The immune response is specific for thyroglobulin, both in terms of the antibody response and T-cell proliferation. In fact, the appearance of lesions can be predicted by the presence of thyroglobulin-specific IgG2b antibody. The disease, moreover, can be transferred adoptively, using spleen cells from iodine-fed donors treated in vitro with iodinated thyroglobulin. The effects of iodine feeding are greater in conventional animals compared with those maintained under specific pathogen-free conditions. Based on T-cell proliferation, it appears that the NOD-H2(h4) strain of mice has innately a greater response to murine thyroglobulin than do other mouse strains and that the proliferation is increased even more by feeding iodine. We suggest, therefore, that the presence of iodine increases the autoantigenic potency of thyroglobulin, a major pathogenic antigen in the induction of Autoimmune Thyroiditis. This animal model provides a unique opportunity for investigating in detail the mechanisms by which an environmental agent can trigger a pathogenic Autoimmune response in a susceptible host.
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iodine induced Autoimmune Thyroiditis in nod h 2h4 mice
Clinical Immunology and Immunopathology, 1996Co-Authors: Linda Rasooly, Lynne C Burek, Noel R. RoseAbstract:Excess iodine ingestion has been implicated in induction and exacerbation of Autoimmune Thyroiditis in human populations and animal models. We studied the time course and sex-related differences in iodine-induced Autoimmune Thyroiditis in NOD-H-2h4 mice. This strain, derived from a cross of NOD with B10.A(4R), spontaneously develops Autoimmune Thyroiditis but not diabetes. NOD-H-2h4 mice were given either plain water or water with 0.05% iodine for 8 weeks. Approximately 54% of female and 70% of male iodine-treated mice developed thyroid lesions, whereas only 1 of 20 control animals had Thyroiditis at this time. Levels of serum thyroxin (T4) were similar in the treatment and control groups. Thyroglobulin-specific antibodies were present in the iodine-treated group after 8 weeks of treatment but antibodies to thyroid peroxidase were not apparent in the serum of any of the animals. Levels of thyroglobulin antibodies increased throughout the 8-week iodine ingestion period; however, no correlation was seen between the levels of total thyroglobulin antibodies and the degree of thyroid infiltration at the time of autopsy. The thyroglobulin antibodies consisted primarily of IgG2a, IgG2b, and IgM antibodies with no detectable IgA, IgG1, or IgG3 thyroglobulin-specific antibodies. The presence of IgG2b thyroglobulin-specific antibodies correlated well with the presence of thyroid lesions.
C. Lynne Burek - One of the best experts on this subject based on the ideXlab platform.
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Invariant NKT Cell Lines Derived from the NOD·H2h4 Mouse Enhance Autoimmune Thyroiditis
Journal of thyroid research, 2011Co-Authors: Rajni Sharma, Patrizio Caturegli, Noel R. Rose, Xiaoguang Fan, C. Lynne BurekAbstract:To study the role of invariant Natural Killer T cell ( iNKT) cells in Autoimmune Thyroiditis, we derived two iNKT cell lines from the spleens of NOD· H2h4 mice, a strain that develops spontaneous Autoimmune Thyroiditis exacerbated by excess dietary iodine. The two lines were CD1d-restricted and expressed CD4+, DX5+, and the Vα4Jα281 gene segment, of the T-cell receptor α locus. Upon stimulation with α-galactosyl-ceramide (α-GalCer), both lines rapidly produced IL-2, IL-4, IFN-γ, IL-10, and TNF-α. Strikingly, a similar cytokine response was also induced by thyroglobulin, one of the most abundant protein in the thyroid gland and a major autoantigen in human Autoimmune Thyroiditis. Transfer of the iNKT cell lines to syngeneic hosts enhanced Autoimmune Thyroiditis. Intraperitoneal injections of α-GalCer in iodine primed mice also induced thyroid disease. This paper reports for the first time that iNKT cells respond to thyroglobulin and enhance Autoimmune Thyroiditis in iodine fed NOD·H2h4 mice.
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Autoimmune Thyroiditis research at Johns Hopkins University.
Immunologic research, 2010Co-Authors: C. Lynne BurekAbstract:Autoimmune Thyroiditis is an organ-specific Autoimmune disorder characterized by infiltration of the thyroid gland by lymphocytic inflammatory cells, often followed by hypothyroidism due to destruction and replacement of the follicular tissue. Dr. Noel Rose and members of his laboratory at Johns Hopkins University have continued to study autoimmunity using Autoimmune Thyroiditis as a model. Autoimmune Thyroiditis is multifactorial, with both genetic and environmental factors involved. We have studied familial association of thyroid antibodies in juveniles with either Autoimmune Thyroiditis or Graves' disease. Epitope analysis of thyroglobulin autoantibodies showed that autoantibodies from unrelated patients with disease had greater similarity of epitope binding than members of their own family. Subclass analysis of thyroglobulin autoantibodies indicated that IgG2 was dominant in Autoimmune Thyroiditis. Much of our work focused around iodine as an environmental trigger of Autoimmune Thyroiditis. We showed that iodination of the human thyroglobulin molecule alters its immunoreactivity. We explored the role of excess iodine ingestion in exacerbating Thyroiditis using the NOD.H2h4 mouse as a model. We found multiple effects of excess iodine, including changing the immunogenicity of the thyroglobulin molecule and the upregulation of ICAM-1 and ROS in the thyrocyte itself. These observations may help to delineate the mechanisms by which iodine exacerbates Thyroiditis and to explain differences in the host response of genetically susceptible individuals compared to those who are resistant to disease.
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Autoimmune Thyroiditis and ROS
Autoimmunity Reviews, 2008Co-Authors: C. Lynne Burek, Noel R. RoseAbstract:Abstract Autoimmune Thyroiditis, also known as chronic lymphocytic or Hashimoto's Thyroiditis, is characterized by infiltration of the thyroid gland by inflammatory cells and production of autoantibodies to thyroid-specific antigens thyroglobulin and thyroperoxidase. It is accompanied by hypothyroidism due to destruction and eventual fibrous replacement of the follicle cells. Autoimmune Thyroiditis is clearly multifactorial in etiology with genetic and environmental factors contributions. Excess dietary Iodine can exacerbate Thyroiditis in genetically susceptible hosts such as the NOD.H2 h4 mouse. In this mouse excess dietary iodine leads to an increased immunogenicity of the thyroglobulin molecule and enhanced expression of ICAM-1 on thyroidal follicle cells. We present evidence here that ICAM-1 expression is enhanced by the elevated generation of reactive oxygen species (ROS). The anti-oxidant diphenyleneiodium (DPI), an inhibitor of NADPH oxidase, reduced both the generation of ROS and of ICAM-1 expression in cultures of NOD.H2 h4 mouse thyrocytes. These results suggest that antioxidants may have therapeutic value in preventing Autoimmune Thyroiditis.
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Linking lodine with Autoimmune Thyroiditis
Environmental Health Perspectives, 1999Co-Authors: Noel R. Rose, Linda Rasooly, Ali M. Saboori, C. Lynne BurekAbstract:A great deal of circumstantial evidence has linked iodine with the rising incidence of Autoimmune Thyroiditis in the United States. In our investigations, we have shown directly that T cells from humans with chronic lymphocytic Thyroiditis proliferate in the presence of iodinated but not in the presence of noniodinated human thyroglobulin. Moreover, the proliferative response is restored when the thyroglobulin is iodinated artificially in vitro. Using a panel of monoclonal antibodies, we found evidence that the presence of iodine induces a number of stereochemical changes in the conformation of the molecule, resulting in the loss of some antigenic determinants and the appearance of others. One prominent determinant was associated with the iodine-containing amino acid thyroxine. Both the number and position of the iodine substituents determine the precise specificity of this epitope. A new model for the study of the role of iodine in inducing thyroid autoimmunity has become available in the form of the nonobese diabetic (NOD)-H2(h4) mouse. This animal develops Autoimmune Thyroiditis spontaneously but in relatively low prevalence. However, if iodine is added to the drinking water, the prevalence and severity of the thyroid lesions increase markedly. The immune response is specific for thyroglobulin, both in terms of the antibody response and T-cell proliferation. In fact, the appearance of lesions can be predicted by the presence of thyroglobulin-specific IgG2b antibody. The disease, moreover, can be transferred adoptively, using spleen cells from iodine-fed donors treated in vitro with iodinated thyroglobulin. The effects of iodine feeding are greater in conventional animals compared with those maintained under specific pathogen-free conditions. Based on T-cell proliferation, it appears that the NOD-H2(h4) strain of mice has innately a greater response to murine thyroglobulin than do other mouse strains and that the proliferation is increased even more by feeding iodine. We suggest, therefore, that the presence of iodine increases the autoantigenic potency of thyroglobulin, a major pathogenic antigen in the induction of Autoimmune Thyroiditis. This animal model provides a unique opportunity for investigating in detail the mechanisms by which an environmental agent can trigger a pathogenic Autoimmune response in a susceptible host.
Héctor M. Targovnik - One of the best experts on this subject based on the ideXlab platform.
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Association of the TGrI29 microsatellite in thyroglobulin gene with Autoimmune Thyroiditis in a Argentinian population: a case–control study
Endocrine, 2010Co-Authors: Viviana Varela, Oscar D. Bruno, Carina M. Rivolta, Sabina Domené, Mariana L. Tellechea, Leonardo Rizzo, Héctor M. TargovnikAbstract:Autoimmune thyroid disease (AITD) is a multifactorial disorder that involves a putative association with thyroid autoantigen-specific and immune regulatory genes, as well as environmental factors. The thyroglobulin gene is the main identified thyroid autoantigen-specific gene associated to Autoimmune Thyroiditis. The aim of this work was to test for evidence of allelic association between Autoimmune Thyroiditis (AT) and thyroglobulin polymorphism markers in Argentinian patients. We studied six polymorphisms distributed throughout all the thyroglobulin gene: four microsatellites (Tgms1, Tgms2, TGrI29, and TGrI30), one insertion/deletion polymorphism (IndelTG-IVS18), and one exonic single nucleotide polymorphism (c.7589G>A) in 100 AT patients and 100 healthy control subjects. No differences in allele and genotype frequencies distribution were observed between Autoimmune Thyroiditis cases and controls for Tgms1, Tgms2, TGrI30, IndelTG-IVS18, and c.7589G>A. However, when we analyzed Autoimmune Thyroiditis patients with the TGrI29 microsatellite we found a significant association between the 197-bp allele and Autoimmune Thyroiditis (33.50% vs. 19.00% in control group) ( P = 0.001). In addition, a significant major prevalence of the 197/201-bp genotype has been also seen in Autoimmune Thyroiditis subjects (59% vs. 24% in control group, P
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Association of the TGrI29 microsatellite in thyroglobulin gene with Autoimmune Thyroiditis in a Argentinian population: a case–control study
Endocrine, 2010Co-Authors: Viviana Varela, Leonardo F. L. Rizzo, Oscar D. Bruno, Carina M. Rivolta, Sabina Domené, Mariana L. Tellechea, Héctor M. TargovnikAbstract:Autoimmune thyroid disease (AITD) is a multifactorial disorder that involves a putative association with thyroid autoantigen-specific and immune regulatory genes, as well as environmental factors. The thyroglobulin gene is the main identified thyroid autoantigen-specific gene associated to Autoimmune Thyroiditis. The aim of this work was to test for evidence of allelic association between Autoimmune Thyroiditis (AT) and thyroglobulin polymorphism markers in Argentinian patients. We studied six polymorphisms distributed throughout all the thyroglobulin gene: four microsatellites (Tgms1, Tgms2, TGrI29, and TGrI30), one insertion/deletion polymorphism (IndelTG-IVS18), and one exonic single nucleotide polymorphism (c.7589G>A) in 100 AT patients and 100 healthy control subjects. No differences in allele and genotype frequencies distribution were observed between Autoimmune Thyroiditis cases and controls for Tgms1, Tgms2, TGrI30, IndelTG-IVS18, and c.7589G>A. However, when we analyzed Autoimmune Thyroiditis patients with the TGrI29 microsatellite we found a significant association between the 197-bp allele and Autoimmune Thyroiditis (33.50% vs. 19.00% in control group) (P = 0.001). In addition, a significant major prevalence of the 197/201-bp genotype has been also seen in Autoimmune Thyroiditis subjects (59% vs. 24% in control group, P < 0.0001). In conclusion, our work showed the association between the thyroglobulin gene and Autoimmune Thyroiditis in Argentinian population and supports the described evidence of thyroglobulin as a thyroid-specific gene linked to AITD.
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Analysis of thyroglobulin gene polymorphisms in patients with Autoimmune Thyroiditis
Endocrine, 2010Co-Authors: Mariela Caputo, Carina M. Rivolta, Teresa Mories, Juan J. Corrales, Purificación Galindo, Rogelio González-sarmiento, Héctor M. Targovnik, José M. Miralles-garcíaAbstract:The Autoimmune thyroid disease is a complex disorder caused by a combination of genetic susceptibility and environmental factors, which are believed to initiate the Autoimmune response to thyroid antigens. Identification of the susceptibility genes has found that unique and diverse genetic factors are in association with Graves’ disease and Autoimmune Thyroiditis. The thyroglobulin gene is an identified thyroid-specific gene associated to Autoimmune thyroid disease and, principally, with Autoimmune Thyroiditis. The aim of this work was to test for evidence of allelic association between Autoimmune Thyroiditis and thyroglobulin polymorphism markers. We studied six polymorphisms distributed throughout all the thyroglobulin gene: four microsatellites (Tgms1, Tgms2, TGrI29 and TGrI30), one insertion/deletion (Indel) polymorphism (IndelTG-IVS18) and one exonic single nucleotide polymorphism (SNP) (c.7589G>A) in 122 patients with Autoimmune Thyroiditis compared with 100 non-related normal subjects. No differences in allele and genotype distribution were observed between Autoimmune Thyroiditis cases and controls for Tgms1, Tgms2, TGrI30, IndelTG-IVS18 and c.7589G>A. However, when we analyzed the patients with the TGrI29 microsatellite we found a significant association between the 199-bp allele and AT (33.7% vs. 24.5% in control group) ( P = 0.0372). In addition, a higher prevalence of the 201-bp allele has been observed in control subjects (47.5% vs. 38.1% in patients group), although not statistically significant ( P = 0.0536). Our work shows the association between the thyroglobulin gene and Autoimmune Thyroiditis and reinforce that thyroglobulin is a thyroid-specific susceptibility gene for this disease.
Oscar D. Bruno - One of the best experts on this subject based on the ideXlab platform.
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Non-Autoimmune Thyroiditis
Medicina, 2014Co-Authors: Leonardo F. L. Rizzo, Daniela L. Mana, Oscar D. BrunoAbstract:The term Thyroiditis comprises a group of thyroid diseases characterized by the presence of inflammation, including Autoimmune and non-Autoimmune entities. It may manifest as an acute illness with severe thyroid pain (subacute Thyroiditis and infectious Thyroiditis), and conditions in which the inflammation is not clinically evident evolving without pain and presenting primarily thyroid dysfunction and/or goiter (drug-induced Thyroiditis and Riedel Thyroiditis). The aim of this review is to provide an updated approach on non-Autoimmune Thyroiditis and its clinical, diagnostic and therapeutic aspects.
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Association of the TGrI29 microsatellite in thyroglobulin gene with Autoimmune Thyroiditis in a Argentinian population: a case–control study
Endocrine, 2010Co-Authors: Viviana Varela, Oscar D. Bruno, Carina M. Rivolta, Sabina Domené, Mariana L. Tellechea, Leonardo Rizzo, Héctor M. TargovnikAbstract:Autoimmune thyroid disease (AITD) is a multifactorial disorder that involves a putative association with thyroid autoantigen-specific and immune regulatory genes, as well as environmental factors. The thyroglobulin gene is the main identified thyroid autoantigen-specific gene associated to Autoimmune Thyroiditis. The aim of this work was to test for evidence of allelic association between Autoimmune Thyroiditis (AT) and thyroglobulin polymorphism markers in Argentinian patients. We studied six polymorphisms distributed throughout all the thyroglobulin gene: four microsatellites (Tgms1, Tgms2, TGrI29, and TGrI30), one insertion/deletion polymorphism (IndelTG-IVS18), and one exonic single nucleotide polymorphism (c.7589G>A) in 100 AT patients and 100 healthy control subjects. No differences in allele and genotype frequencies distribution were observed between Autoimmune Thyroiditis cases and controls for Tgms1, Tgms2, TGrI30, IndelTG-IVS18, and c.7589G>A. However, when we analyzed Autoimmune Thyroiditis patients with the TGrI29 microsatellite we found a significant association between the 197-bp allele and Autoimmune Thyroiditis (33.50% vs. 19.00% in control group) ( P = 0.001). In addition, a significant major prevalence of the 197/201-bp genotype has been also seen in Autoimmune Thyroiditis subjects (59% vs. 24% in control group, P
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Association of the TGrI29 microsatellite in thyroglobulin gene with Autoimmune Thyroiditis in a Argentinian population: a case–control study
Endocrine, 2010Co-Authors: Viviana Varela, Leonardo F. L. Rizzo, Oscar D. Bruno, Carina M. Rivolta, Sabina Domené, Mariana L. Tellechea, Héctor M. TargovnikAbstract:Autoimmune thyroid disease (AITD) is a multifactorial disorder that involves a putative association with thyroid autoantigen-specific and immune regulatory genes, as well as environmental factors. The thyroglobulin gene is the main identified thyroid autoantigen-specific gene associated to Autoimmune Thyroiditis. The aim of this work was to test for evidence of allelic association between Autoimmune Thyroiditis (AT) and thyroglobulin polymorphism markers in Argentinian patients. We studied six polymorphisms distributed throughout all the thyroglobulin gene: four microsatellites (Tgms1, Tgms2, TGrI29, and TGrI30), one insertion/deletion polymorphism (IndelTG-IVS18), and one exonic single nucleotide polymorphism (c.7589G>A) in 100 AT patients and 100 healthy control subjects. No differences in allele and genotype frequencies distribution were observed between Autoimmune Thyroiditis cases and controls for Tgms1, Tgms2, TGrI30, IndelTG-IVS18, and c.7589G>A. However, when we analyzed Autoimmune Thyroiditis patients with the TGrI29 microsatellite we found a significant association between the 197-bp allele and Autoimmune Thyroiditis (33.50% vs. 19.00% in control group) (P = 0.001). In addition, a significant major prevalence of the 197/201-bp genotype has been also seen in Autoimmune Thyroiditis subjects (59% vs. 24% in control group, P < 0.0001). In conclusion, our work showed the association between the thyroglobulin gene and Autoimmune Thyroiditis in Argentinian population and supports the described evidence of thyroglobulin as a thyroid-specific gene linked to AITD.
