Circulating thyroid hormone autoantibodies

Benvenga, Salvatore; Trimarchi, Francesco; Robbins, Jacob

doi:10.1007/bf03347008

Cited by 57 publications

(29 citation statements)

References 107 publications

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“…THB Abs recognize thyroxine (T4) or triiodothyronine (T3) residues on distinct hormonogenic sites of thyroglobulin (Tg) and are being viewed as a subset of Tg-reactive autoantibodies. Development of THB Abs does not usually result in systemic hypothyroidism because of the ability of thyroid-pituitary feedback mechanisms to compensate for hormone neutralization (1,2). However, THB Abs are clinically quite important because they interfere with the measurement of T3 and/or T4 and may occasionally hinder appropriate diagnosis and treatment (3)(4)(5).…”

mentioning

confidence: 99%

Thyroxine-Binding Antibodies Inhibit T Cell Recognition of a Pathogenic Thyroglobulin Epitope

Dai

Eliades

Carayanniotis

et al. 2005

The Journal of Immunology

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Thyroid hormone-binding (THB) Abs are frequently detected in autoimmune thyroid disorders but it is unknown whether they can exert immunoregulatory effects. We report that a THB mAb recognizing the 5′ iodine atom of the outer phenolic ring of thyroxine (T4) can block T cell recognition of the pathogenic thyroglobulin (Tg) peptide (2549–2560) that contains T4 at aa position 2553 (T4(2553)). Following peptide binding to the MHC groove, the THB mAb inhibited activation of the Ak-restricted, T4(2553)-specific, mouse T cell hybridoma clone 3.47, which does not recognize other T4-containing epitopes or noniodinated peptide analogues. Addition of the same THB mAb to T4(2553)-pulsed splenocytes largely inhibited specific activation of T4(2553)-primed lymph node cells and significantly reduced their capacity to adoptively transfer thyroiditis to naive CBA/J mice. These data demonstrate that some THB Abs can block recognition of iodine-containing Tg epitopes by autoaggressive T cells and support the view that such Abs may influence the development or maintenance of thyroid disease.

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confidence: 99%

Thyroxine-Binding Antibodies Inhibit T Cell Recognition of a Pathogenic Thyroglobulin Epitope

Dai

Eliades

Carayanniotis

et al. 2005

The Journal of Immunology

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“…Clinically, anti-thyroid hormone autoantibodies in patients' sera interfere with radioimmunoassay results of thyroid hormones (1)(2)(3). This interference confuses clinicians on the evaluation of the actual patients' thyroid state.…”

Section: Discussionmentioning

confidence: 99%

“…It has been knownthat the presence of circulating antithyroid hormone antibodies can cause an apparent but artifactual effect on the result of radioimmunoassay (RIA) for serum total and free serum thyroxine (T4) and triiodothyronine (T3) (1)(2)(3). Earlier studies have documented that such autoantibodies are present not only in various thyroidal diseases but also in nonthyroidal disorders such as Waldenstrom macroglobulinemia (4), hepatocellular carcinoma (5) and systemic lupus erythematosus (SLE) (6).…”

Section: Introductionmentioning

confidence: 99%

Autoimmune Hepatitis and Hypothyroidism Associated with Anti-thyroid Hormone Autoantibodies.

et al. 1993

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A 40-year-old hypothyroid female who had been treated with synthetic thyroxine was admitted to our hospital in October 1988 due to abnormal liver function tests. She had low serum free triiodothyronine (T3; 2.3pg/ml) and high serum thyrotropin (TSH; 20.8 /iU/ml) concentrations. On the other hand, the serum free thyroxine (FT4) level was inappropriately high, being 2.46 ng/dl. Immuneprecipitation of radiolabeled thyroid hormones with her serum disclosed the binding of 125I-T3 and 125I-T4 to the extent of 9.5% and ll.3%, respectively (normal ranges for 125I-T3 and 125I-T4 binding are less than 6.3% and 5.9%, respectively). 125I-T4 binding to the patient's serum gammaglobulin was completely displaced with the addition of unlabeled T4. Further examination disclosed that anti-T4 antibodies in her serum belong to IgG k class immunoglobulin. (Internal Medicine 32: 21-25, 1993)

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“…46,47 We have previously shown that the 55H8 mAb, representing this subset, recognizes the 5΄ iodine atom of the outer phenolic ring of T4 within the T4(2553) peptide, even after the peptide is bound to the major histocompatibility complex (MHC) (A k ) groove. 48 Thus, 55H8 inhibits activation of T4(2553)-specific T cells and significantly reduces their capacity to transfer EAT to naive mice.…”

Section: B3 Regulation Of Tg-specific T Cell Reactivity By Antibodiementioning

confidence: 99%

Molecular parameters linking thyroglobulin iodination with autoimmune thyroiditis

Carayanniotis¹

2011

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Increased iodide intake has been linked to the development of hypothyroidism and/or autoimmune thyroiditis in humans and animals, but the mechanisms involved remain poorly understood. Increased ingestion of iodide is likely to have pleiotropic effects on either metabolic or immunological processes. Within the latter domain, recent interest has been focused on two areas: a) the role of iodinated peptides in thyroglobulin (tg)-the molecular site of biosynthesis and storage of iodotyrosines and iodothyronines-in triggering an autoimmune cascade, and b) the role of iodine-induced apoptosis/necrosis of thyrocytes in the disease process. this review presents a brief summary of recent findings in these research areas.

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Circulating thyroid hormone autoantibodies

Cited by 57 publications

References 107 publications

Thyroxine-Binding Antibodies Inhibit T Cell Recognition of a Pathogenic Thyroglobulin Epitope

Thyroxine-Binding Antibodies Inhibit T Cell Recognition of a Pathogenic Thyroglobulin Epitope

Autoimmune Hepatitis and Hypothyroidism Associated with Anti-thyroid Hormone Autoantibodies.

Molecular parameters linking thyroglobulin iodination with autoimmune thyroiditis

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