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The Cross-Knit between Immune Cells and Thyroid Function in Autoimmune Thyroid Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 October 2024 | Viewed by 5691

Special Issue Editors


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Guest Editor
Endocrine Unit, ASST dei Sette Laghi, 21100 Varese, Italy
Interests: thyroid autoimmunity; Graves' disease; Hashimoto's thyroiditis; Vitamina D; Selenium; obesity

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Guest Editor
Immunology and General Pathology Laboratory, Department of Biotechnology and Life Sciences, University of Insubria, 21100 Varese, Italy
Interests: human tumor angiogenesis; innate immune cells in the tumor microenvironment; natural killer cells and macrophages in human cancers; evaluating novel immunotherapeutic interventions based on immunocitokynes TNF and IL-2, in combination setting against tumor development and metastasis in preclinical tumor murine models.
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Special Issue Information

Dear Colleagues,

Autoimmune thyroid disorders, which include chronic autoimmune thyroiditis (CAT) and Graves’ disease (GD), represent the most common organ-specific autoimmune diseases. In CAT, the immune infiltration of the thyroid gland causes follicular cell damage and hypothyroidism, whereas the synthesis of antibodies stimulating the thyrotropin receptor induces thyrocyte hyperplasia and hyperthyroidism in GD. The influence of thyroid hormones on immune cells’ activation, phenotype, and function has emerged in preclinical studies. However, the mutual effect of high/low thyroid hormone levels in the progression and perpetuation of autoimmunity has not been clarified yet. Given the absence of treatments for both hypo- and hyperthyroidism able to target the underlying immune process, this crosstalk might be crucial for the development of new therapeutic approaches. We therefore invite researchers working in the fields of immunology and endocrinology to submit original research articles or reviews discussing the most recent advancements on this topic.

Dr. Daniela Gallo
Dr. Lorenzo Mortara
Guest Editors

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Keywords

  • autoimmune thyroid disorders
  • innate immune cells
  • adaptive immune cells
  • thyrotropin
  • thyroid hormones

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Published Papers (2 papers)

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Review

16 pages, 1014 KiB  
Review
Regulatory T Cells in the Pathogenesis of Graves’ Disease
by Natasa Kustrimovic, Daniela Gallo, Eliana Piantanida, Luigi Bartalena, Adriana Lai, Nicola Zerbinati, Maria Laura Tanda and Lorenzo Mortara
Int. J. Mol. Sci. 2023, 24(22), 16432; https://doi.org/10.3390/ijms242216432 - 17 Nov 2023
Cited by 2 | Viewed by 2863
Abstract
Maintaining a delicate balance between the prompt immune response to pathogens and tolerance towards self-antigens and commensals is crucial for health. T regulatory (Treg) cells are pivotal in preserving self-tolerance, serving as negative regulators of inflammation through the secretion of anti-inflammatory cytokines, interleukin-2 [...] Read more.
Maintaining a delicate balance between the prompt immune response to pathogens and tolerance towards self-antigens and commensals is crucial for health. T regulatory (Treg) cells are pivotal in preserving self-tolerance, serving as negative regulators of inflammation through the secretion of anti-inflammatory cytokines, interleukin-2 neutralization, and direct suppression of effector T cells. Graves’ disease (GD) is a thyroid-specific autoimmune disorder primarily attributed to the breakdown of tolerance to the thyroid-stimulating hormone receptor. Given the limitations of currently available GD treatments, identifying potential pathogenetic factors for pharmacological targeting is of paramount importance. Both functional impairment and frequency reduction of Tregs seem likely in GD pathogenesis. Genome-wide association studies in GD have identified polymorphisms of genes involved in Tregs’ functions, such as CD25 (interleukin 2 receptor), and Forkhead box protein P3 (FOXP3). Clinical studies have reported both functional impairment and a reduction in Treg frequency or suppressive actions in GD, although their precise involvement remains a subject of debate. This review begins with an overview of Treg phenotype and functions, subsequently delves into the pathophysiology of GD and into the existing literature concerning the role of Tregs and the balance between Tregs and T helper 17 cells in GD, and finally explores the ongoing studies on target therapies for GD. Full article
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20 pages, 982 KiB  
Review
Innate Immunity in Autoimmune Thyroid Disease during Pregnancy
by Tatjana Bogović Crnčić, Neva Girotto, Maja Ilić Tomaš, Ines Krištofić, Sanja Klobučar, Lara Batičić, Božena Ćurko-Cofek and Vlatka Sotošek
Int. J. Mol. Sci. 2023, 24(20), 15442; https://doi.org/10.3390/ijms242015442 - 22 Oct 2023
Cited by 3 | Viewed by 2316
Abstract
Autoimmune thyroid disease (AITD) is the most common organ-specific autoimmune disorder clinically presented as Hashimoto thyroiditis (HT) and Graves’ disease (GD). The pathogenesis of AITD is caused by an inappropriate immune response related to genetic, non-genetic, and environmental factors. Pregnancy is one of [...] Read more.
Autoimmune thyroid disease (AITD) is the most common organ-specific autoimmune disorder clinically presented as Hashimoto thyroiditis (HT) and Graves’ disease (GD). The pathogenesis of AITD is caused by an inappropriate immune response related to genetic, non-genetic, and environmental factors. Pregnancy is one of the factors that have a great influence on the function of the thyroid gland because of the increased metabolic demand and the effects of hormones related to pregnancy. During pregnancy, an adaptation of the maternal immune system occurs, especially of the innate immune system engaged in maintaining adaptive immunity in the tolerant state, preventing the rejection of the fetus. Pregnancy-related hormonal changes (estrogen, progesterone, hCG) may modulate the activity of innate immune cells, potentially worsening the course of AITD during pregnancy. This especially applies to NK cells, which are associated with exacerbation of HD and GD. On the other hand, previous thyroid disorders can affect fertility and cause adverse outcomes of pregnancy, such as placental abruption, spontaneous abortion, and premature delivery. Additionally, it can cause fetal growth retardation and may contribute to impaired neuropsychological development of the fetus. Therefore, maintaining the thyroid equilibrium in women of reproductive age and in pregnant women is of the highest importance. Full article
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