Thyroid Autoimmunity and Environment

Tanda, Maria Laura; Piantanida, Eliana; Lai, Aiyun; Lombardi, V.; Mule, I. Dalle; Liparulo, Luigi; Pariani, Nadia; Bartalena, Luigi

doi:10.1055/s-0029-1215568

Cited by 51 publications

(39 citation statements)

References 81 publications

(110 reference statements)

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“…A number of studies provide evidence that allergyassociated mechanisms can contribute to the pathogenesis of autoimmune diseases such as AITD (Tanda et al 2009). An association was found between an allergic constitution (asthma, atopic eczema) and AITD, with OR values of 2.54 (95% CI, 1.16-5.57) and 2.95 (95% CI, 1.37-6.34) (Moens et al 1984).…”

Section: Discussionmentioning

confidence: 99%

The −112G > A polymorphism of the secretoglobin 3A2 (SCGB3A2) gene encoding uteroglobin-related protein 1 (UGRP1) increases risk for the development of Graves’ disease in subsets of patients with elevated levels of immunoglobulin E

et al. 2010

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The human secretoglobin 3A2 (SCGB3A2) gene encoding secretory uteroglobin-related protein 1 (UGRP1) resides on the chromosome region 5q31-33 that harbors a susceptibility locus to several autoimmune and inflammatory diseases, including asthma and Graves' disease (GD). Recently, association between the marker rs1368408 (-112G >A), located in the promoter region of the SCGB3A2 gene, and susceptibility to GD was found in Chinese and UK Caucasians. The study aim was to evaluate whether this polymorphism confers GD susceptibility in a large population cohort comprising 1,474 Russian GD patients and 1,619 controls. The marker rs1368408 was studied using a TaqMan allele discrimination assay. Serum levels of UGRP1 and immunoglobulin E (IgE) were assessed using enzyme-linked immunosorbent assay (ELISA) analyses. Association between the allele A of SCGB3A2 and a higher risk of GD (odds ratio [OR] = 1.33, P = 2.9 × 10(-5)) was shown. Both affected and non-affected carriers of the higher risk genotype A/A had significantly decreased levels of serum UGRP1 compared to the subjects homozygous for G/G (93 ± 37 pg/ml vs. 132 ± 45 pg/ml, P = 0.0011 for GD patients; 77 ± 28 pg/ml vs. 119 ± 33 pg/ml, P = 0.0019 for controls). Serum IgE levels were significantly higher in non-affected subjects homozygous for A/A compared to control individuals homozygous for G/G (153 ± 46 IU/ml vs. 122 ± 40 IU/ml, P = 0.0095). Our data suggest that the carriage of the SCGB3A2 -112A/A variant increases the risk for GD in subsets of patients with elevated levels of IgE, a hallmark of allergic asthma. Therefore, the SCGB3A2 -112G >A polymorphism may be considered as a likely marker linking susceptibility to allergy/asthma and GD on chromosome 5q31-33.

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Section: Discussionmentioning

confidence: 99%

The −112G > A polymorphism of the secretoglobin 3A2 (SCGB3A2) gene encoding uteroglobin-related protein 1 (UGRP1) increases risk for the development of Graves’ disease in subsets of patients with elevated levels of immunoglobulin E

et al. 2010

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“…IFNα, interleukin-2, lithium, amiodarone, and highly active antiretroviral therapy (HAART) are the agents most commonly associated with thyroid dysfunction (29). …”

Section: Environmental Factors and Aitdmentioning

confidence: 99%

Cutting Edge: The Etiology of Autoimmune Thyroid Diseases

Eschler

Hasham

Tomer

2011

Clinic Rev Allerg Immunol

104

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Significant progress has been made in our understanding of the mechanisms leading to autoimmune thyroid diseases (AITD). For the first time we are beginning to unravel these mechanisms at the molecular level. AITD, including Graves' disease (GD) and Hashimoto's thyroiditis (HT), are common autoimmune diseases affecting the thyroid. They have a complex etiology that involves genetic and environmental influences. Seven genes have been shown to contribute to the etiology of AITD. The first AITD gene discovered, HLA-DR3, is associated with both GD and HT. More recently this association was dissected at the molecular level when it was shown that substitution of the neutral amino acids Ala or Gln with arginine at position beta 74 in the HLA-DR peptide binding pocket is the specific sequence change causing AITD. Non-MHC genes that confer susceptibility to AITD can be classified into two groups: 1) immune regulatory genes (e.g. CD40, CTLA-4, PTPN22); 2) thyroid specific genes -thyroglobulin, and TSH receptor genes. These genes interact with environmental factors, such as infection, likely through epigenetic mechanisms to trigger disease. In this review we summarize the latest findings on disease susceptibility and modulation by environmental factors.

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“…The relationship between inflammation and the presence of microchimerism could be indicative of this theory 90 . Fetal intrathyroidal cells, even immune cells, could therefore be a reflection of an ongoing local immune reaction without active participation 91 . Due to damage to the blood vessels, fetal cells could leak out into the damaged tissue without having an active role in tissue damage or repair 54 .…”

Section: Innocentmentioning

confidence: 99%

Fetal microchimeric cells in autoimmune thyroid diseases

Lepez¹,

Vandewoestyne²,

Deforce³

2013

Chimerism

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Autoimmune thyroid diseases (AITD) show a female predominance, with an increased incidence in the years following parturition. Fetal microchimerism has been suggested to play a role in the pathogenesis of AITD. However, only the presence of fetal microchimeric cells in blood and in the thyroid gland of these patients has been proven, but not an actual active role in AITD. Is fetal microchimerism harmful for the thyroid gland by initiating a Graft versus Host reaction (GvHR) or being the target of a Host versus Graft reaction (HvGR)? Is fetal microchimerism beneficial for the thyroid gland by being a part of tissue repair or are fetal cells just innocent bystanders in the process of autoimmunity? This review explores every hypothesis concerning the role of fetal microchimerism in AITD.

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Thyroid Autoimmunity and Environment

Cited by 51 publications

References 81 publications

The −112G > A polymorphism of the secretoglobin 3A2 (SCGB3A2) gene encoding uteroglobin-related protein 1 (UGRP1) increases risk for the development of Graves’ disease in subsets of patients with elevated levels of immunoglobulin E

The −112G > A polymorphism of the secretoglobin 3A2 (SCGB3A2) gene encoding uteroglobin-related protein 1 (UGRP1) increases risk for the development of Graves’ disease in subsets of patients with elevated levels of immunoglobulin E

Cutting Edge: The Etiology of Autoimmune Thyroid Diseases

Fetal microchimeric cells in autoimmune thyroid diseases

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