Vitamin D supply influences negatively the serum IL-6 and IL-17A levels in Hashimoto’s thyroiditis, while positively the serum antibody levels against thyroid peroxidase and TSH receptor in Graves’ disease

2020 ◽  
Author(s):  
Ildikó Molnár ◽  
Zoltán Nagy
Keyword(s):  
Vitamin D ◽  
Hashimoto’S Thyroiditis ◽  
Serum Antibody ◽  
Tsh Receptor ◽  
Hashimoto's Thyroiditis ◽  
Thyroid Peroxidase ◽  
Graves Disease ◽  
Antibody Levels

scholarly journals Studies in Mice Deficient for the Autoimmune Regulator (Aire) and Transgenic for the Thyrotropin Receptor Reveal a Role for Aire in Tolerance for Thyroid Autoantigens

Endocrinology ◽  
2009 ◽  
Vol 150 (6) ◽  
pp. 2948-2956 ◽  
Author(s):  
Alexander V. Misharin ◽  
Yuji Nagayama ◽  
Holly A. Aliesky ◽  
Basil Rapoport ◽  
Sandra M. McLachlan
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Hashimoto's Thyroiditis ◽  
Thyroid Peroxidase ◽  
Graves Disease ◽  
Binding Motif ◽  
Wild Type ◽  
Autoimmune Regulator ◽  
The Third ◽  
A Subunit ◽  
Thyroid Autoantigens

The autoimmune regulator (Aire) mediates central tolerance for many autoantigens, and autoimmunity occurs spontaneously in Aire-deficient humans and mice. Using a mouse model of Graves’ disease, we investigated the role of Aire in tolerance to the TSH receptor (TSHR) in Aire-deficient and wild-type mice (hyperthyroid-susceptible BALB/c background). Mice were immunized three times with TSHR A-subunit expressing adenovirus. The lack of Aire did not influence T-cell responses to TSHR protein or TSHR peptides. However, antibody levels were higher in Aire-deficient than wild-type mice after the second (but not the third) immunization. After the third immunization, hyperthyroidism persisted in a higher proportion of Aire-deficient than wild-type mice. Aire-deficient mice were crossed with transgenic strains expressing high or low-intrathyroidal levels of human TSHR A subunits. In the low-expressor transgenics, Aire deficiency had the same effect on the pattern of the TSHR antibody response to immunization as in nontransgenics, although the amplitude of the response was lower in the transgenics. High-expressor A-subunit transgenics were unresponsive to immunization. We examined intrathymic expression of murine TSHR, thyroglobulin, and thyroid peroxidase (TPO), the latter two being the dominant autoantigens in Hashimoto’s thyroiditis (particularly TPO). Expression of the TSHR and thyroglobulin were reduced in the absence of Aire. Dramatically, thymic expression of TPO was nearly abolished. In contrast, the human A-subunit transgene, lacking a potential Aire-binding motif, was unaffected. Our findings provide insight into how varying intrathymic autoantigen expression may modulate thyroid autoimmunity and suggest that Aire deficiency may contribute more to developing Hashimoto’s thyroiditis than Graves’ disease.

Determination of serum neopterin levels in patients with autoimmune thyroid diseases

2012 ◽  
Vol 153 (29) ◽  
pp. 1127-1131 ◽  
Author(s):  
Csaba Balázs ◽  
Boglárka Türke ◽  
Árpád Vámos
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Thyroid Stimulating Hormone ◽  
Hashimoto's Thyroiditis ◽  
Graves Disease ◽  
Important Indicator ◽  
Autoimmune Thyroid ◽  
Serum Neopterin ◽  
Antibody Levels ◽  
Stimulating Hormone

An elevated serum level of neopterin indicates the activation of the cellular immune system. Aim: The objective was to find a correlation in autoimmune thyroid patients between neopterin levels and the clinical stage of the disease and to examine whether neopterin can predict the relapse of the disease. Methods: Serum neopterin, thyroid stimulating hormone, free thyroxine, free triiodothyronine, anti-thyroglobulin and anti-thyroid peroxidase antibody levels were determined in 137 patients with Graves’ disease (in different stages), 25 with Hashimoto’s thyroiditis and 14 with toxic adenoma. Results: The neopterin levels were significantly higher in patients with Graves’ disease (hyper-, eu-, hypothyroidism and relapsed hyperthyroidism) and Hashimoto’s thyroiditis. Positive correlation was found between neopterin and anti-thyroglobulin and anti-tyhroid peroxidase antibody levels, but no correlation was detected between neopterin levels and thyroid hormones, thyroid stimulating hormone values and antibodies against thyroid stimulating hormone receptors. Conclusions: Higher level of serum neopterin reflects an underlying autoimmune process, and does not correlate with changes in thyroid hormone levels. Determination of neopterin level can be an important indicator in the exacerbation of autoimmune processes. Orv. Hetil., 2012, 153, 1127–1131.

COMPARISON OF THYROID ANTIGENS BY THE EXPERIMENTAL PRODUCTION OF PRECIPITATING ANTIBODIES TO HUMAN THYROID FRACTIONS AND THE IDENTIFICATION OF AN ANTIBODY WHICH COMPETES WITH LONG-ACTING THYROID STIMULATOR (LATS) FOR THYROID BINDING

1977 ◽  
Vol 84 (4) ◽  
pp. 759-767 ◽  
Author(s):  
Christian von Westarp ◽  
Andrew J. S. Knox ◽  
Vas V. Row ◽  
Robert Volpé
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Tsh Receptor ◽  
Human Thyroid ◽  
Hashimoto's Thyroiditis ◽  
Graves Disease ◽  
Experimental Production ◽  
Long Acting ◽  
First Time ◽  
Good Animal Model

ABSTRACT Antibodies were raised to various sub-cellular fractions of human thyroids, (of Graves' disease, Hashimoto's thyroiditis, and non-toxic goitre). With one exception it was found that antibodies to the Graves' thyroid fractions cross-reacted with both the non-toxic goitre and Hashimoto's thyroiditis fractions. This exception was in the antiserum to the Graves' 105 000 × g pellet (Gr4) which contained an antibody (A-1) that could not be absorbed by either the non-toxic goitre (NTG) or the Hashimoto's (H) thyroid preparations. The antibody-antigen reaction between A-1 and Gr4 could be blocked by the addition of LATS (or TSH) to the antigen, thus suggesting that A-1 might be a LATS-like immunoglobulin. These results suggest that the TSH receptor may be antigenic and that an antibody to this receptor can be produced in vivo. Production of such an antibody to the TSH receptor would permit the development for the first time of a good animal model of Graves' disease.

scholarly journals The Link between Graves’ Disease and Hashimoto’s Thyroiditis: A Role for Regulatory T Cells

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 5724-5733 ◽  
Author(s):  
Sandra M. McLachlan ◽  
Yuji Nagayama ◽  
Pavel N. Pichurin ◽  
Yumiko Mizutori ◽  
Chun-Rong Chen ◽  
...  
Keyword(s):  
T Cells ◽  
Antibody Response ◽  
Hashimoto’S Thyroiditis ◽  
Lymphocytic Infiltration ◽  
Hashimoto's Thyroiditis ◽  
Thyroid Peroxidase ◽  
Graves Disease ◽  
Wild Type ◽  
Treg Depletion ◽  
A Subunit

Hyperthyroidism in Graves’ disease is caused by thyroid-stimulating autoantibodies to the TSH receptor (TSHR), whereas hypothyroidism in Hashimoto’s thyroiditis is associated with thyroid peroxidase and thyroglobulin autoantibodies. In some Graves’ patients, thyroiditis becomes sufficiently extensive to cure the hyperthyroidism with resultant hypothyroidism. Factors determining the balance between these two diseases, the commonest organ-specific autoimmune diseases affecting humans, are unknown. Serendipitous findings in transgenic BALB/c mice, with the human TSHR A-subunit targeted to the thyroid, shed light on this relationship. Of three transgenic lines, two expressed high levels and one expressed low intrathyroidal A-subunit levels (Hi- and Lo-transgenics, respectively). Transgenics and wild-type littermates were depleted of T regulatory cells (Treg) using antibodies to CD25 (CD4+ T cells) or CD122 (CD8+ T cells) before TSHR-adenovirus immunization. Regardless of Treg depletion, high-expressor transgenics remained tolerant to A-subunit-adenovirus immunization (no TSHR antibodies and no hyperthyroidism). Tolerance was broken in low-transgenics, although TSHR antibody levels were lower than in wild-type littermates and no mice became hyperthyroid. Treg depletion before immunization did not significantly alter the TSHR antibody response. However, Treg depletion (particularly CD25) induced thyroid lymphocytic infiltrates in Lo-transgenics with transient or permanent hypothyroidism (low T4, elevated TSH). Neither thyroid lymphocytic infiltration nor hypothyroidism developed in similarly treated wild-type littermates. Remarkably, lymphocytic infiltration was associated with intermolecular spreading of the TSHR antibody response to other self thyroid antigens, murine thyroid peroxidase and thyroglobulin. These data suggest a role for Treg in the natural progression of hyperthyroid Graves’ disease to Hashimoto’s thyroiditis and hypothyroidism in humans.

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