The role of hereditary and environmental factors in autoimmune thyroid diseases

2012 ◽  
Vol 153 (26) ◽  
pp. 1013-1022 ◽  
Author(s):  
Csaba Balázs

Autoimmune thyroid diseases are the most common organ-specific autoimmune disorders affecting 5% to 10% of the population in Western countries. The clinical presentation varies from hyperthyroidism in Graves’ disease to hypothyroidism in Hashimoto’s thyroiditis. While the exact etiology of thyroid autoimmunity is not known, the interaction between genetic susceptibility and environmental factors appears to be of fundamental importance to initiate the process of thyroid autoimmunity. The identified autoimmune thyroid disease susceptibility genes include immune-modulating genes, such as the major histocompatibility complex, and thyroid-specific genes, including TSH receptor, thyroglobulin and thyroid peroxidase. The majority of the anti-TSH-receptor antibodies have a stimulating capacity and are responsible for hyperthyroidism. The anti-thyroglobulin- and anti-thyroid peroxidase antibodies belonging to the catalytic type of antibodies destroy the thyrocytes resulting in hypothyroidism. The appearance of anti-thyroid peroxidase antibodies precedes the induction of thyroiditis and the manifestation of hypothyroidism. The molecular analysis of thyroglobulin gene polymorphism is important in the mechanism of autoimmune thyroiditis. The autoantigen presentation by major histocompatibility complex molecules is a key point of the autoimmune mechanism. It has been shown that a HLA-DR variant containing arginine at position 74 of the DRβ1 chain confers a strong genetic susceptibility to autoimmune thyroid diseases, Graves’ disease and Hashimoto’s thyroiditis, while glutamine at position DRβ1-74 is protective. Human thyroglobulin 2098 peptide represents a strong and specific DRβ1-Arg74 binder, while a non-binding control peptide, thyroglobulin 2766 fails to induce this response. Moreover, thyroglobulin 2098 stimulated T-cells from individuals who were positive for thyroglobulin antibodies, demonstrating that thyroglobulin 2098 is an immunogenic peptide capable of being presented in vivo and activating T-cells in autoimmune thyroid diseases. Taken together these findings suggest that thyroglobulin 2098, a strong and specific binder to the disease-associated HLA-DRβ1-Arg74, is a major human T-cell epitope and it participates in the pathomechanism of the autoimmune thyroid disease. The exact nature of the role of environmental factors in the autoimmune thyroid disease is still not well known, but the importance of several factors such as iodine, drugs and infections has been reported. Further knowledge of the precise mechanisms of interaction between environmental factors and genes in inducing thyroid autoimmunity could result in the development of new strategies for diagnosis, prevention and treatment. Orv. Hetil., 2012, 153, 1013–1022.

2021 ◽  
Author(s):  
Ewa Czubek ◽  
Piotr Romaniuk ◽  
Klaudia Alcer ◽  
Mirjana Varjacic

Abstract Background: Autoimmune thyroid diseases are the most common diseases in humans. Their pathogenesis is complex. Patients are searching for ways of coping with them condition, including diet modifications. The aim of this study was to assess the role of medical personnel in shaping eating habits in patients with autoimmune thyroid disease based on experiences declared by patients. Methods: There were 208 people that took part in the study, of which 205 were qualified for final analysis. The results showed that patients most often choose online sources, while medical personnel rank second as the source of information on dietary recommendations.Results: People with thyroid disease are statistically more likely to use dietitian advice than people without thyroid disease. The highest percentage of respondents decided to modify their nutrition due to their own initiative. In addition, patients with autoimmune thyroid disease are statistically more likely to consider changing their diet to improve their well-being. The connection between the source of advice and modification of eating behaviour was also noted.Conclusion: Thanks to the joint effort of medical staff, patients can receive reliable knowledge about their disease, treatment and nutrition adapted to their needs.Trial registration: approved by the Bioethics Committee of Medical University of Silesia in Katowice (opinion no.: PCN/0022/KB1/80/2).


2019 ◽  
Vol 14 (4) ◽  
pp. 192-205 ◽  
Author(s):  
Ekaterina A. Troshina ◽  
Evgeniya S. Senyushkina ◽  
Maria A. Terekhova

The past few years have been actively discussing the role of individual macro- and micronutrients as factors regulating the functional activity of organs and systems and reducing the risk of developing a number of diseases, including thyroid diseases. Selenium is one of the most important and intensively studied at present microelements. According to several studies, its low plasma level is associated with an increased risk of developing autoimmune thyroid diseases. In animal experiments, it was shown that a combined deficiency of selenium and iodine leads to more pronounced hypothyroidism than iodine deficiency alone. Some authors believe that cretinism in the newborn is a consequence of the combined deficiency of these two elements in the mother. It is also important that the optimal level of selenium is necessary both to initiate an immune response and to regulate an excessive immune response, as well as chronic inflammation. The review article discusses the relationship between selenium and thyroid pathology, discusses the role of selenium in the physiology of the thyroid gland and in the development of autoimmune diseases. The biochemical aspects of the pathogenesis of thyroid disease are presented.


2009 ◽  
Vol 2009 ◽  
pp. 1-5 ◽  
Author(s):  
Huy A. Tran ◽  
Glenn E. M. Reeves

Autoimmune thyroid diseases are common manifestations of hepatitis C infection, exacerbated by interferon-based treatment. However, the occurrence and pattern of thyroid disease in the short/medium term following the completion of IFN-based therapy is relatively unknown and there are very few previous reports regarding the specific spectrum of autoimmune thyroid disease that may follow such therapy. We hereby report 3 cases which demonstrate the range of thyroid diseases that may occur following interferon therapy. The hypothesis advanced is that in the pathogenesis of these conditions there must be both triggering and sustaining mechanisms as thyroid diseases occur well outside the immediate effect window of pegylated interferon. This paper suggests the need to continue thyroid surveillance in IFN-treated HCV patients following the completion of therapy, perhaps for the first 6 months.


2003 ◽  
Vol 31 (1) ◽  
pp. 21-36 ◽  
Author(s):  
DA Chistiakov ◽  
RI Turakulov

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.


Medicina ◽  
2021 ◽  
Vol 57 (6) ◽  
pp. 621
Author(s):  
Efstratios Kardalas ◽  
Spyridoula Maraka ◽  
Maria Papagianni ◽  
George Paltoglou ◽  
Charalampos Siristatidis ◽  
...  

Transforming growth factor beta (TGF-β), as a master regulator of immune response, is deeply implicated in the complex pathophysiology and development of autoimmune thyroid diseases. Based on the close interplay between thyroid autoimmunity and TGF-β, scientific interest was shifted to the understanding of the possible role of this molecule regarding the diagnosis, prognosis, and therapy of these diseases. The main aim of this review is to present research data about possible treatment options based on the role of TGF-β in thyroid autoimmunity. Suggested TGF-β-mediated therapeutic strategies regarding autoimmune thyroid diseases include either the enhancement of its immunosuppressive role or inhibition of its facilitatory role in thyroid autoimmunity. For example, the application of hr-TGF-β can be used to bolster the inhibitory role of TGF-β regarding the development of thyroid diseases, whereas anti-TGF-β antibodies and similar molecules could impede its immune-promoting effects by blocking different levels of TGF-β biosynthesis and activation pathways. In conclusion, TGF-β could evolve to a promising, novel therapeutic tool for thyroid autoimmunity.


2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
M. A. Iddah ◽  
B. N. Macharia

Purpose of Review. Studies have been published in the field of autoimmune thyroid diseases since January 2005. The review is organized into areas of etiology, autoimmune features, autoantibodies, mechanism of thyroid cell injury, B-cell responses, and T-cell responses. Also it reviews the diagnosis and the relationship between autoimmune thyroid disease, neoplasm, and kidney disorders. Recent Findings. Autoimmune thyroid diseases have been reported in people living in different parts of the world including North America, Europe, Baalkans, Asia, Middle East, South America, and Africa though the reported figures do not fully reflect the number of people infected per year. Cases are unrecognized due to inaccurate diagnosis and hence are treated as other diseases. However, the most recent studies have shown that the human autoimmune thyroid diseases (AITDs) affect up to 5% of the general population and are seen mostly in women between 30 and 50 years. Summary. Autoimmune thyroid disease is the result of a complex interaction between genetic and environmental factors. Overall, this review has expanded our understanding of the mechanism involved in pathogenesis of AITD and the relationship between autoimmune thyroid disease, neoplasm, and kidney disease. It has opened new lines of investigations that will ultimately result in a better clinical practice.


2011 ◽  
Vol 2 (2) ◽  
pp. 139-154 ◽  
Author(s):  
E. Kiseleva ◽  
K. Mikhailopulo ◽  
O. Sviridov ◽  
G. Novik ◽  
Y. Knirel ◽  
...  

During recent years, researchers have been focusing on the concept of an infectious etiology of autoimmune diseases. The most discussed theory is molecular mimicry, i.e. the emergence of autoreactive clones of T- and B-lymphocytes as a result of cross-immune response to homologous bacterial or viral antigen. Information on the role of probiotic microorganisms (PM) in the molecular mechanisms of autoimmune thyroid diseases (ATD) is limited. Using proteins and immunogenic peptides databanks and relevant computer programs, the homology between the amino acid sequences of thyroid peroxidase (TPO) and thyroglobulin (Tg), which are potential B- and T-cell epitopes of these antigens, and proteins of bifidobacteria and lactobacilli was established. Moreover, we have found components of cells of Bifidobacterium bifidum 791, Bifidobacterium adolescentis 94 BIM, Bifidobacterium longum B379M and Lactobacillus plantarum B-01 that selectively bind human antibodies to TPO (anti-TPO) and antibodies to Tg (anti-Tg) and compete with natural antigens for the binding of anti-TPO and anti-Tg in ELISA. Additionally, a three-fold difference was observed between the probability of detecting antibodies (Abs) to the antigens of L. plantarum B-01 and B. bifidum 791 in serum samples containing and those not containing anti-TPO. On the whole, our data are arguments in favour of the assumption of the possible role of PM of the genera Bifidobacterium and Lactobacillus in triggering ATD by the mechanism of molecular mimicry. The data obtained in silico and in vitro should be proven by use of animal models and clinical studies for extrapolations to the whole body. Possible antigenic properties of components/proteins of bifidobacteria and lactobacilli, selectively binding anti-TPO and anti-Tg should be taken into consideration. Natural human Abs to these bacterial components are probably able to cross-react with the TPO and Tg in the ELISA for detection of anti-TPO and anti-Tg, which are serologic markers of ATD. It can lead to unspecific false positive results and, hence, to an incorrect diagnosis.


2012 ◽  
Vol 56 (9) ◽  
pp. 677-682 ◽  
Author(s):  
Ana Rosa P. Quidute ◽  
Eduardo Vasconcelos de Freitas ◽  
Tadeu Gonçalves de Lima ◽  
Ana Márcia Lima Feitosa ◽  
Joyce Paiva dos Santos ◽  
...  

Many cases have been published showing a co-existence of autoimmune thyroid diseases (AITDs) and other autoimmune diseases. About a quarter of patients with achalasia have a concurrent thyroid disease, most commonly associated with hypothyroidism. Although relatively rare, the association of achalasia and hyperthyroidism requires attention. The physiopathology of Grave's Disease (GD) involves B- and T-mediator lymphocytes, which have an affinity for known thyroid antigens: thyroglobulin, thyroid-peroxidase, and thyrotrophin receptor. Currently, however, the real physiopathogenesis of achalasia continues to be unknown. Some important findings are suggestive of an autoimmune mechanism: significant infiltration of the myoenteric plexus by monocytes, presence of the class II-Human Histocompatibility Complex DQwl antigen and antibodies to myoenteric neurons. The present case reports a patient who, despite testing negative for Chagas' disease, had achalasia, progressed to developing significant wasting and worsening of his quality of life, was later diagnosed with hyperthyroidism. After endoscopic esophageal dilatation and radioiodine ablation of the thyroid gland, there was great improvement in the patient clinical condition. Arq Bras Endocrinol Metab. 2012;56(9):677-82


2017 ◽  
Vol 95 (6) ◽  
pp. 524-534
Author(s):  
B. I. Gel’tser ◽  
V. V. Zdor ◽  
Vladimir N. Kotel’nikov

Modern scientific literature contains few reports concerning the influence of target therapy on pathogenetic factors of autoimmune thyroid diseases (AITD). Despite a large number of hypotheses of AITD pathogenesis, the only well established fact is the starting stage of Graves disease (GD) and autoimmune thyroiditis (AIT) is the loss of tolerance to thyroid autoantigens and the final stage is production of autoantibodies to them. Up to 75-80% of the patients with GD have antibodies against thyroid peroxidase and only few of them have anti-thyroglobulin antibodies more characteristic of AIT. Thyrotropin releasing hormone (TRH) is known to stimulate T-lymphocyte production via local effect on insulin-like growth factor (IGF). Modern studies confirm the important role of cytokines in immunopathogenesis of GD and AIT. Moreover, excess activation of this system in AITD provides a basis for the development of specific therapeutic approaches to personified pharmacotherapy. The effectiveness of anti-cytokine therapy of GD and AIT was demonstrated in animal experiments. Studies of therapy targeted on orbital and thyroid autoantigens in AITD are currently underway. The existence of specific receptors and the ability of immunocompetent cells to produce neuropeptides create prerequisites for their participation in intercellular cooperative processes. It can be supposed, by analogy with the influence of hormones and neuromediators on immunocytes, that neurohormones act on them via specific receptors with the involvement of cyclic nucleotides. It opens up opportunity for targeted correction of these relationships. Further studies of immunopathogenetic mechanisms of GD and AIT for better understanding the role of interaction between inborn and acquired immunity, its regulation, and intersystem transmission of signals in the development of these diseases are needed to realize modern strategies of their target therapy.


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