Association of Serum Antithyroid Antibodies with Lymphocytic Infiltration of the Thyroid Gland: Studies of Seventy Autopsied Cases*

Yoshida, Hiroshi; Amino, Nobuyuki; Yagawa, Kanichi; Uemura, Kazuhiro; Satoh, Masanobu; Miyai, Kiyoshi; Kumahara, Yuichi

doi:10.1210/jcem-46-6-859

Cited by 238 publications

(103 citation statements)

References 16 publications

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“…In agreement with our results, thyroid antibodies decreased markedly or disappeared after withdrawal of iodine. In a histological study, association between the presence of thyroid antibodies and lymphocyte infiltration of the gland was demonstrated (31), and histological features of 28 antibody-positive patients with iodine-induced hypothyroidism included diffuse lymphocyte infiltration with follicles of reduced size containing sparse colloid (32). Along with our cytological findings, cessation of intake of iodine led to normalisation of thyroid function, decreased antibody titre, and disappearance of lymphocyte infiltration.…”

Section: European Journal Of Endocrinology (1998) 139supporting

confidence: 74%

Iodide induces thyroid autoimmunity in patients with endemic goitre: a randomised, double-blind, placebo-controlled trial

Kahaly¹,

Dienes²,

Beyer³

et al. 1998

European Journal of Endocrinology

124

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Objective: Iodine is essential for normal thyroid function and the majority of individuals tolerate a wide range of dietary levels. However, a subset of individuals, on exposure to iodine, develop thyroid dysfunction. In this double-blind trial, we evaluated the efficacy and tolerability of low-dose iodine compared with those of levo-thyroxine (T 4 ) in patients with endemic goitre. Methods: Sixty-two patients were assigned randomly to groups to receive iodine (0.5 mg/day) or T 4 (0.125 mg/day) for 6 months. Subsequently, both groups were subject to placebo for another 6 months. Thyroid sonography, determination of thyroid-related hormones and antibodies, and urinary excretion of iodine were carried out at baseline and at 1, 6 and 12 months. Results: At 6 months, markedly increased urinary values of iodine were found in patients receiving iodine (36 mg/24 h at baseline, 415 mg/24 h at 6 months) compared with those receiving T 4 (47 mg/ 24 h at baseline, 165 mg/24 h at 6 months; P < 0.0001 compared with iodine group). T 4 administration engendered a greater (P < 0.01) decrease in thyroid volume (from 32 ml to 17 ml, P < 0.0001) than did intake of iodine (33 ml to 21 ml, P < 0.005). High microsomal and thyroglobulin autoantibody titres were present in six of 31 patients (19%) receiving iodine, and iodine-induced hypo-and hyperthyroidism developed in four and two of them, respectively. Fine-needle biopsy revealed marked lymphocyte infiltration in all six. After withdrawal of iodine, thyroid dysfunction remitted spontaneously and antibody titres and lymphocyte infiltration decreased markedly. Follow-up of these six patients for an additional 3 years showed normalisation of antibody titres in four of them. Conclusion: Although nearly comparable results were obtained with both treatment regimens regarding thyroid size, partly reversible iodine-induced thyroid dysfunction and autoimmunity were observed among patients with endemic goitre.

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Section: European Journal Of Endocrinology (1998) 139supporting

confidence: 74%

Iodide induces thyroid autoimmunity in patients with endemic goitre: a randomised, double-blind, placebo-controlled trial

Kahaly¹,

Dienes²,

Beyer³

et al. 1998

European Journal of Endocrinology

124

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“…Serum thyroid antibodies in subjects without overt thyroid disease may indicate that lymphocytes have infiltrated the thyroid gland [17], and it has been reported that a signifieant part of thyroid autoantibodies are produeed by intrathyroidal lymphocytes [18 20J. The number oi lymphocytes obtained from the thyroid tissue was correlated with the scrum titres oi MeAb and TgAb in our patients with autoimmune thyroid disease.…”

Section: Discussionmentioning

confidence: 55%

Intrathyroidal lymphocyte subsets, including unusual CD4+CD8+ cells and CD3loTCRαβ1o/-CD4−CD8−cells, in autoimmune thyroid disease

Iwatani

Hidaka

Matsuzuka

et al. 1993

Clinical and Experimental Immunology

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SUMMARY Intralhyroidal lymphocyte subsets were analysed in 13 cuthyroid patients with autoimmune thyroid disease by two‐colour flow cytometry and compared with subsets in peripheral blood. In both Graves' and Hashimoto's diseases, proportions of intrathyroidal CDS B cells were higher than in peripheral blood. The numbers of such cells were correlated with serum levels of anti‐thyroid microsomal antibodies. Proportions of T cells bearing αβ chains of T cell receptors (TCRαβ+T; Tαβ) and CD16+CD57+ natural killer (NK) cells were lower in the thyroid, but proportions of CD3hiTCRαβ− TCRγδ+ (Tγδ) cells were not different. Proportions of CD4+ Leu‐8+ helper T cells and CD4+CD57+ germinal centre T cells were higher and proportions of CD4+ Leu‐8+ suppressor‐inducer T cells and CD8+CD57+ or CD+ CD11b+ suppressor T cells were lower than in the blood in both diseases. Proportions of CD5+ B cells were high in Graves' disease, and proportions of CD8+ CD11b− cytotoxic T cells were high in Hashimoto's disease. Unexpectedly, CD4+ CD8+ cells and CD3.TCRαβ CD4−CDS cells were present in thyroid tissues of both diseases. These findings suggest that: (i) an imbalance in the numbers of regulatory T cells and of NK cells that had appeared in the thyroid resulted in the proliferation of CDS B cells, which were related to thyroid autoantibody production; (ii) CD5+ B cells and cytotoxic T cells are important for the different pathological features in Graves' and Hashimoto's diseases, respectively; and (iii) intrathyroidal CD4+CD8+ cells and CD31oTCRαβlo‐CD4−CD8− cells may be related to the pathogenesis of autoimmune thyroid disease.

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“…A utoimmune thyroid diseases (AITDs) are characterized by the production of pathogenic thyroid autoantibodies and lymphocyte infiltration (1,2). Autoantibodies against various thyroid antigens such as thyroid peroxidase (TPO), thyroglobulin (Tg), sodium iodide symporter (SLC5A5: NIS), and Pendred syndrome gene (SLC26A4: Pendrin) are present in the sera of patients with Hashimoto's thyroiditis (3,4).…”

Section: Introductionmentioning

confidence: 99%

Demonstration of Innate Immune Responses in the Thyroid Gland: Potential to Sense Danger and a Possible Trigger for Autoimmune Reactions

Kawashima

Yamazaki²,

Hara

et al. 2013

Thyroid

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Background: Autoimmune thyroid disease is an archetypal organ-specific autoimmune disorder that is characterized by the production of thyroid autoantibodies and lymphocytic infiltration into the thyroid. However, the underlying mechanisms by which specific thyroid antibodies are produced are largely unknown. Recent studies have shown that innate immune responses affect both the phenotype and the severity of autoimmune reactions. Moreover, it appears that even non-immune cells, including thyroid cells, have an ability to launch such responses. The aim of this study was to conduct a more detailed analysis of innate immune responses of the thyroid upon stimulation with various ''non-self'' and ''self'' factors that might contribute to the initiation of autoimmune reactions. Methods: We used rat thyroid FRTL-5 cells, human thyroid cells, and mice to investigate the effects of various pathogen-associated molecular patterns (PAMPs), danger-associated molecular patterns (DAMPs), and iodide on gene expression and function that were related to innate immune responses. Results: RT-PCR analysis showed that both rat and human thyroid cells expressed mRNAs for Toll-like receptors (TLRs) that sense PAMPs. Stimulation of thyrocytes with TLR ligands resulted in activation of the interferon-beta (IFN-b) promoter and the nuclear factor kappa-light-chain-enhancer of activated B cells (NFjB)-dependent promoter. As a result, pro-inflammatory cytokines, chemokines, and type I interferons were produced. Similar activation was observed when thyroid cells were stimulated with double-stranded DNA, one of the typical DAMPs. In addition to these PAMPs and DAMPs, treatment of thyroid cells with high concentrations of iodide increased mRNA expression of various cytokines. Conclusion: We show that thyroid cells express functional sensors for exogenous and endogenous dangers, and that they are capable of launching innate immune responses without the assistance of immune cells. Such responses may relate to the development of thyroiditis, which in turn may trigger autoimmune reactions.

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Association of Serum Antithyroid Antibodies with Lymphocytic Infiltration of the Thyroid Gland: Studies of Seventy Autopsied Cases*

Cited by 238 publications

References 16 publications

Iodide induces thyroid autoimmunity in patients with endemic goitre: a randomised, double-blind, placebo-controlled trial

Iodide induces thyroid autoimmunity in patients with endemic goitre: a randomised, double-blind, placebo-controlled trial

Intrathyroidal lymphocyte subsets, including unusual CD4+CD8+ cells and CD3loTCRαβ1o/-CD4−CD8−cells, in autoimmune thyroid disease

Demonstration of Innate Immune Responses in the Thyroid Gland: Potential to Sense Danger and a Possible Trigger for Autoimmune Reactions

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