Tolerance and autoimmunity
Gabriel Virella in Medical Immunology, 2019
Latent viral infections are believed to be responsible for the development of many autoimmune disorders. Latent infection is commonly associated with integration of the viral genome into the host chromosomes. While integrated viruses very seldom enter a full replicative cycle and do not cause cytotoxicity, they can interfere, directly or indirectly, with several functions of the infected cells. T-cell activation secondary to an inapparent viral infection has the potential to induce autoimmunity secondary to the release of interferon-γ and TNF, both known to be potent inducers of MHC-II antigen expression. The increased expression of class-II MHC antigens would then create optimal conditions for the onset of an autoimmune response directed against MHC-II–self peptide complexes. Such a mechanism has been proposed to explain the onset of autoimmune thyroiditis. An unknown nonlytic virus would cause T-lymphocyte activation in the thyroid gland, followed by increased expression of MHC-II and thyroid-derived peptides, and finally, an antithyroid immune reaction would develop.
Other Inherited Disorders of the Thyroid System
Geraldo Medeiros-Neto, John Bruton Stanbury in Inherited Disorders of the Thyroid System, 2019
The more common thyroid disorders are also characteristically familial in incidence.15 This was recognized in the early descriptions of Graves’ disease. Chronic autoimmune thyroiditis (Hashimoto’s thyroiditis) also runs in families. Familial occurrence of differentiated thyroid carcinoma has also been recently recognized. Simple sporadic goiter often has family clustering. In all these conditions the mode of inheritance is presumably multifactorial and polygenic, that is, more than one gene generate the trait, their effects are cumulative, and environmental factors are important in phenotypic expression. The disease is expressed only when a critical combination of genetic and environmental factors is realized. Thus, it is the risk of the tendency to the disorder rather than the disorder itself that is inherited.
Immunopathology
Constantin A. Bona, Francisco A. Bonilla in Textbook of Immunology, 2019
Strong familial patterns are observed in humans with autoimmune thyroiditis or systemic lupus erythematosus. However, several related individuals may have circulating autoantibodies of the same specificity, yet only one or a few of them may develop overt symptoms. This discordance even extends to monozygotic twins, clearly indicating that genetic factors are only one component in the etiology of autoimmune disease. Prominent among the genes implicated in human autoimmune disease are those within the HLA complex, antibody and T cell receptor variable region genes, and cytokine and cytokine receptor genes. With respect to antibody variable regions, many attempts have been made to identify polymorphisms associated with autoimmunity, or biased usage of V genes in autoantibodies. A single human antibody VH gene, VH4-21, ia found in high frequency among human autoantibodies analyzed to date. These include polyspecific antibodies, as well as antibodies which bind to IgG (rheumatoid factors), red blood cells (cold agglutinins), DNA, and muscle antigens. The significance of this high frequency for the etiology of autoimmunity is not yet clear since this gene is highly represented in normal B cells as well.
Vitamin D deficiency, insulin resistance and thyroid dysfunction in obese patients: is inflammation the common link?
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2018
Nicoleta Răcătăianu, Nicoleta Valentina Leach, Sorana D. Bolboacă, Angela Cozma, Eleonora Dronca, Ana Valea, Alina Silaghi, Ana Maria Bîlc, Cristina Ghervan
In the investigated obese group, vitamin D deficiency was severe and correlated negatively with BMI. During the cold season, vitamin D deficiency was significantly more pronounced compared to the warm season and significantly correlated with VFT. At a 15 ng/mL cut-off value, vitamin D negatively correlated with systemic inflammation assessed by serum MCP-1. Moreover, MCP-1 increased with HOMA-IR and proved to be a predictive factor for vitamin D deficiency. This suggests that the systemic inflammation can also be a risk factor for vitamin D deficiency and sustaining a bidirectional relation between vitamin D deficiency and inflammation. Furthermore, systemic inflammation increases the severity and occurrence of autoimmune thyroiditis. Vitamin D deficiency is the single independent factor associated with the presence of Hashimoto’s thyroiditis with multivariate regression analysis.
Omalizumab therapy in a patient with cronic spontaneous urticaria, ulcerative colitis, hypereosinophilia and prurigo Besnier: a case report
Published in Journal of Dermatological Treatment, 2018
T. Grieco, C. Chello, V. Faina, V. V. Gomes, L. Alei, A. Sernicola, V. Panasiti, S. Calvieri
The patient was admitted to hospital for laboratory tests. Blood tests showed hyper-eosinophilia (9.2%), D-dimer elevation (869 µg/L fibrinogen-equivalent units [FEU], normal range 50–420), polyclonal γ-globulin elevation (19.3%) and high levels of thyroid peroxidase autoantibodies (TPO 49 UI/ml (reference values 0.00–34.00), with normal values of thyroid hormones (TSH 1.47 µUI/ml, reference values 0.27–4.20, FT3 2.2 pg/ml, reference values 2.00–4.40) except for low levels of FT4 (0.85 ng/dl, reference values 0.93–1.70). Data suggested the presence of autoimmune thyroiditis. In addition, levels of vitamin D in the lower range, with increased parathyroid hormone (PTH): vitamin D3 7 ng/mL (reference values 6.23–49.9), PTH 69.8 pg/ml (reference values 15–65). Folic acid was deficient: 2.8 ng/mL (reference values 3.80–16.00) and vitamin B12 increased (>2000 pg/ml (reference values 191.00–663.00). Total IgE levels was increased (1243.00 U/ml, reference values 4.00–100.00), while antinuclear antibodies (ANA) and extractable nuclear antigen antibodies (ENA) were negative.
Gluten-free diet attenuates the impact of exogenous vitamin D on thyroid autoimmunity in young women with autoimmune thyroiditis: a pilot study
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2022
Robert Krysiak, Karolina Kowalcze, Bogusław Okopień
Autoimmune (Hashimoto’s thyroiditis) is the most common thyroid disease, the major cause of thyroid hypofunction in developed countries and one of the most common human disorders worldwide [1,2]. The disease is associated with antibody-mediated cytotoxicity and apoptosis, which leads to the progressive loss of follicular cells, the consequence of which is replacement of the thyroid tissue by lymphoid lymphocytic infiltrate, fibrotic reaction and hypothyroidism [3]. Although highly prevalent, autoimmune thyroiditis still remains a poorly understood and understudied disorder of unknown pathogenesis, awaiting prevention strategies and new modes of treatment. There are some arguments suggesting, however, that the risk of autoimmune thyroiditis and its severity may be affected by vitamin D status and gluten intake.
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