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PubMed2026

Cell Type-Resolved Causal Inference and Spatial Transcriptomic Integration Reveal Immune-Specific Genetic Drivers of Autoimmune and Malignant Thyroid Disease.

BACKGROUND: Thyroid diseases, including autoimmune thyroid disease (AITD) and thyroid cancer, are characterized by immune dysregulation, yet the cell type-specific genetic mechanisms underlying these conditions remain poorly understood. Most genome-wide association studies (GWAS) have relied on bulk tissue expression quantitative trait loci (eQTL), which cannot resolve the heterogeneity of immune cell populations. METHODS: We performed two-sample Mendelian randomization (MR) analyses using single-cell cis-eQTLs from 14 immune cell subtypes (OneK1K cohort) as instrumental variables against GWAS summary statistics for four thyroid outcomes: autoimmune hyperthyroidism, autoimmune hypothyroidism, thyroid cancer and autoimmune thyroiditis. Causal associations were validated through Bayesian colocalization, phenome-wide association analysis (PheWAS) and multi-layered transcriptomic validation encompassing spatial transcriptomics of AITD tissue (GSE248205), bulk RNA-seq of thyroid cancer (GSE3678) and single-cell RNA-seq of thyroid tumours (GSE250521). gsMap spatial LD score regression was applied to map disease heritability onto spatial tissue architecture. RESULTS: We identified six Bonferroni-significant causal gene-cell type pairs for autoimmune hyperthyroidism, including protective effects of ABHD16A in na&#xef;ve/immature B cells (OR&#xa0;=&#xa0;0.440), HIST1H3H in CD8 NC T cells (OR&#xa0;=&#xa0;0.324), HMGN4 in NK recruiting cells (OR&#xa0;=&#xa0;0.556) and ZKSCAN4 in CD8 S100B T cells (OR&#xa0;=&#xa0;0.427), with five pairs showing strong colocalization (PP.H4 &#x2265; 86%). Three pairs reached significance for autoimmune hypothyroidism, including a risk association of HLA-F in CD4 NC T cells (OR&#xa0;=&#xa0;1.139). For autoimmune thyroiditis, FAM134B/RETREG1 showed consistent suggestive protective associations across both CD4 and CD8 NC T cells (PP.H4 &#x2265; 90% for both), suggesting a possible involvement of ER phagy regulation in thyroiditis susceptibility. Thyroid cancer showed a suggestive association with HLA-G in classical monocytes (OR&#xa0;=&#xa0;1.899, PP.H4&#xa0;=&#xa0;53%). Spatial transcriptomic validation demonstrated progressive immune infiltration from control tissue to Graves' disease to Hashimoto's thyroiditis (7.7%-15.7%, 46.1%-54.1%, respectively) and strong spatial correlation between target gene expression and corresponding cell type enrichment (e.g., plasma cell-HLA-DQB1: r&#xa0;=&#xa0;0.491, p < 10-300). HLA-G was independently validated in thyroid cancer bulk (log2fc&#xa0;=&#xa0;0.542, p&#xa0;=&#xa0;9.51&#xa0;&#xd7;&#xa0;10-3, AUC&#xa0;=&#xa0;0.857) and single-cell datasets. PheWAS revealed no significant associations detected for the core candidates. gsMap identified significant enrichment of autoimmune hypothyroidism heritability in gastrointestinal tract, adrenal gland and adipose tissue (all Bonferroni p < 0.002). CONCLUSIONS: This study establishes a multi-scale analytical framework integrating cell type-resolved genetic inference with spatial tissue validation, revealing distinct immunogenetic architectures underlying autoimmune versus malignant thyroid disease. Protective genetic programs in autoimmune hyperthyroidism converge on chromatin remodelling (HIST1H3H, HMGN4, ZKSCAN4) and lipid metabolism (ABHD16A) across lymphocyte subsets, whereas thyroid cancer risk involves immune escape mediated by HLA-G in myeloid cells. The ER-phagy receptor RETREG1 represents a candidate pathway warranting further investigation in autoimmune thyroiditis. These findings provide genetically supported, cell type-specific therapeutic targets and demonstrate a generalizable strategy for dissecting the immune-mediated mechanisms of complex thyroid diseases.

Mendelian randomization↗
PubMed2006

[Epidemiology of Basedow disease and other thyroid diseases].

Basedow disease is one of several representative thyroid diseases. According to information from Japan's Ministry of Health, Labour and Welfare, it is estimated that there were a total of about 130,000 patients (32,000 male 98,000 female, sex ratio of 1 : 3) of thyrotoxicosis in Japan during 2002. This number accounts for about 0.1% of the entire population of Japan. Several reports based on data from medical examinations provide higher prevalence rates. A survey of subclinical thyroid diseases is now in progress. There are reports of cases of progression from subclinical status to overt status, which suggests that the number of affected individuals becomes higher. Epidemiological data are still insufficient. Disease registry systems and medical examination data should be further improved.

Age Distribution↗
PubMed1983

T lymphocyte subsets in autoimmune thyroid diseases and subacute thyroiditis detected with monoclonal antibodies.

Peripheral T lymphocyte subsets were analysed with monoclonal antibodies, by highly standardized fluorescence-activated cell sorter analysis instead of manual counting by the indirect immunofluorescence method, in autoimmune thyroid diseases and subacute thyroiditis. Total lymphocyte counts were increased in patients with thyrotoxic Graves' disease and subacute thyroiditis. The percentage of total T (Leu 1) cells was significantly lower in patients with thyrotoxic Graves' disease and Hashimoto's disease with destructive thyrotoxicosis than in normal subjects. No significant changes were observed in the percentages of suppressor-cytotoxic T (Leu 2a) cells or helper-inducer T (Leu 3a) cells or in the Leu 3a-Leu 2a ratio in different groups of patients. There were no correlations between the percentages of E rosette-forming cells and Leu 1 cells and between the percentages of T gamma cells and Leu 2a cells in normal subjects and patients. The peak position of fluorescence intensity of Leu 2a cells showed a significant sex difference even in normal controls. The most important finding was a significant decrease in the peak position of Leu 2a cells in patients with thyrotoxic Graves' disease and with hypothyroid or thyrotoxic Hashimoto's disease. These findings indicate the significant association of qualitative, but not quantitative, abnormality of suppressor-cytotoxic T (Leu 2a) cells with thyroid dysfunction in autoimmune thyroid diseases.

Adult↗
PubMed1994

Coeliac disease and autoimmune thyroid disease.

A well defined cohort of coeliac patients was studied prospectively to assess the prevalence of coexisting thyroid disease and positive thyroid autoantibodies. Comparison with epidemiological data on the prevalence of coeliac disease in a neighbouring area suggested that few adult coeliac patients had been missed. Overall, 14% of the coeliac patients had thyroid disease: 10.3% were hypothyroid and 3.7% hyperthyroid, both significantly more than expected. There were significantly more coeliac disease patients with thyroid autoantibodies than expected--11% had thyroglobulin antibodies and 15% had thyroid microsomal antibodies. This association is clinically important. Three patients are described in whom the coexistence of coeliac disease and hypothyroidism led to diagnostic difficulties and delay of treatment.

Adult↗
PubMed1982

The incidence of occult thyroid disease associated with thyroid antibodies identified on routine autoantibody screening.

The presence of thyroid microsomal and/or thyroglobulin antibodies has been recorded over a 2 year period of 15 000 consecutive autoimmune profile request. Where there had been no initial clinical suspicion of thyroid diseases, 332 requests showed positive thyroid antibodies, and of these 63 (19%) had abnormal in vitro thyroid function tests (TFT). No differences were observed between the abnormal and normal groups with respect to the presence of different autoantibodies or to the age and sex distributions. Of these subjects with clinically unsuspected hypothyroidism but with abnormal TFTs, 29% were commenced on thyroxine therapy and experienced a symptomatic improvement, 25% remain well on no therapy and 9% continue on no treatment but with symptoms possibly attributable to hypothyroidism. 3% became clinically hypothyroid during a follow-up period of 2 years. 5% died of unrelated causes and there was inadequate follow-up information on the remainder. This study provides further confirmation that when thyroid antibodies, and in particular thyroid microsomal antibody, are found unexpectedly, a significant proportion of patients will have biochemical evidence of hypothyroidism and may benefit from appropriate treatment.

Autoantibodies↗
PubMedDate not supplied

Plasma and erythrocyte magnesium concentrations in thyroid disease: relation to thyroid function and the duration of illness.

To clarify magnesium metabolism in thyroid dysfunction, plasma and erythrocyte magnesium concentrations (P-Mg, E-Mg) were determined in patients with untreated thyroid diseases and their relations to thyroid hormone levels and the duration of illness were examined. P-Mg was significantly lower in hyperthyroid patients than in euthyroid or hypothyroid individuals. E-Mg was significantly higher in hypothyroid patients than in hyperthyroid or euthyroid individuals. In the entire series of 84 subjects, both P-Mg and E-Mg showed significant negative correlations with thyroid hormone levels, but the correlations were greater in P-Mg than E-Mg. In hyperthyroid patients, both P-Mg and E-Mg were negatively correlated with the duration of illness, but this correlation was greater in E-Mg than P-Mg. Also, both P-Mg and E-Mg were significantly higher in patients with destructive thyroiditis with a short duration (0.5 months) such as subacute or painless thyroiditis than in patients with Graves' disease (4.9 months). These results suggest that magnesium metabolism in thyroid dysfunction is affected not only by thyroid hormone levels but also by the duration of illness.

Acute Disease↗
PubMed1986

Serological evidence for the role of bacterial infections in the pathogenesis of thyroid diseases.

Subacute thyroiditis is generally believed to be of viral origin, and infection is also suspected of playing a role as a triggering factor in the pathogenesis of autoimmune thyroid diseases. We have measured a broad spectrum of bacterial and viral antibodies in paired sera of 32 patients with thyroid disease of recent onset. The data indicate a preceding infection in 14 (44%) of the patients, enterobacterial in 5, streptococcal in 4 and staphylococcal in 2. A viral infection was suggested in 6 patients, in each case caused by different agents; 3 of them also showed evidence of a bacterial infection. Patients with positive microbial serology were found in all diagnostic groups, including subacute thyroiditis, Graves' disease and Hashimoto's disease. These results suggest an association between a preceding bacterial infection and the development of thyroid disease in some patients.

Adult↗
PubMedDate not supplied

[Thyroid microcarcinoma in benign thyroid diseases].

INTRODUCTION: Thyroid microcarcinoma is a malignant thyroid tumor with potential multifocality and a maximum of 1 cm of diameter. This carcinoma has been discovered more frequently like incidentaloma. AIM OF THE STUDY: To appraise the incidence of MCT in the benign thyroid diseases and the advantages offered from the total thyroidectomy, performed for benign diffused thyroid diseases, which surgical treatment "therapeutic" performed for these malignant tumors. MATERIALS AND METHODS: The study was conducted on 600 patients operated with total thyroidectomy for benign thyroid disease, admitted from 1999 to 2003. RESULTS: All patients were alive and free of disease at last control. DISCUSSION: The MCT is a carcinoma that presents frequently a behavior little malignant and a good prognosis. His principal characteristic is the absence of clinical demonstrations. Therefore his discovery, almost always accidental on a thyroid removed for other pathology, it has signaled by histologic study CONCLUSIONS: Thyroid microcarcinoma is a slow growing tumor, with a good prognosis and with a good disease-free survival. It can present a better aggressiveness for his multifocal localization and invasion. Therefore total thyroidectomy can be considered best treatment and also be surgical treatment oncologically correct for this tumor.

Carcinoma, Papillary↗
PubMed1989

Coexpression of cytokeratins and vimentin in normal and diseased thyroid glands. Lack of diagnostic utility of vimentin immunostaining.

We documented the coexpression of cytokeratins and vimentin in epithelial cells of the thyroid gland in 100 samples examined from 65 patients. These included normal, inflammatory, and neoplastic tissues that were routinely fixed in formalin and embedded in paraffin. The number of epithelial cells coexpressing the two intermediate filament proteins as well as the subcellular compartmentalization of vimentin immunoreactivity did not correlate with the various conditions of the thyroid gland. Therefore, we conclude that the immunolocalization of vimentin does not represent a useful adjunct tool for the histopathological diagnosis of thyroid diseases.

Humans↗
PubMed2005

[Diagnosis of autoimmune thyroid disease].

Autoimmune thyroid disease (AITD) is the most common organ specific autoimmune disorder usually resulting in dysfunction (hyperfunction, hypofunction or both) of the thyroid gland. The syndromes comprising autoimmune thyroid disease are many intimately related illnesses: Graves' disease with goitre, hyperthyroidism and, in many patients, associated ophthalmopathy, Hashimoto's thyroiditis with goitre and euthyroidism or hypothyroidism but also thyroid dysfunction occurring independently of pregnancy and in 5-6% of postpartum women and thyroiditides induced by different drugs and other environmental influences. The immunological mechanisms involved in these diseases are closely related, while the phenotypes probably differ because of the specific type of immunological response that occurs. The syndromes are connected together by their similar thyroid pathology, similar immune mechanisms, co-occurrence in family groups, and transition from one clinical picture to another within the same individual over time. In some patients, other organ specific and nonorgan specific autoimmune syndromes are associated with autoimmune thyroid disease, including pernicious anemia, vitiligo, myasthenia gravis, primary adrenal autoimmune disease, celiac disease, rheumatoid arthritis or lupus. Thyroid peroxydase, TPO, the primary enzyme involved in thyroid hormonogenesis, was initially identified in 1959 as the 'thyroid microsomal antigenn. It is uncertain whether TPO autoantibodies or TPO-specific T cells are the primary cause of thyroid inflammation, which can lead, in some individuals, to thyroid failure and hypothyroidism. TPOAbs are the hallmark of AITB and are present in almost all patients with Hashimoto's thyroiditis, in two-thirds of patients with postpartum thyroiditis and also in 75% of patients with Graves' hyperthyroidism. The antibodies are mainly produced by lymphocytic infiltrate in the thyroid gland and only to a small extent by regional lymph nodes or the bone marrow. Unlike antibodies against thyroglobulin (Tg), TPO antibodies are capable of inducing antibody-dependent cell-mediated cytotoxicity. Antibodies to TSH-R mimic the function of TSH, and cause disease by binding to the TSH-R and stimulating (or inhibiting) thyroid cells. The TSHR, a member of the G protein-coupled receptor family with seven membrane-spanning segments. Patients with autoimmune thyroid disease may have both stimulating and blocking antibodies in their sera, the clinical picture being the result of the relative potency of each species; blocking antibodies seem more common in Graves' patients with ophthalmopathy compared to those without this complication. The major T cell epitopes are heterogeneous and T cell reactivity against certain TSH-R epitopes has been present in high proportion in normal subjects. More diversified response to TSH-R, with heterogeneity of epitope recognition by TSAb, is predictive of likely remission after antithyroid drug treatment for Graves' disease.

Autoimmune Diseases↗
PubMed1994

Anti-thyroid peroxidase (anti-TPO) antibodies in thyroid diseases, non-thyroidal illness and controls. Clinical validity of a new commercial method for detection of anti-TPO (thyroid microsomal) autoantibodies.

The identification of the thyroid peroxidase (TPO) as the main antigen of the thyroid microsomal fraction has enabled the development of a sensitive and specific assay for detection of the corresponding autoantibodies. We evaluated the diagnostic validity of the anti-TPO assay in 303 patients with different types of thyroid disease and in controls. Clearly elevated anti-TPO values (anti-TPO > 500 units/ml) were found in 59% of patients with thyroiditis but in none of the controls or the patients with non-thyroidal illness. The mean anti-TPO levels in these two control groups were 26 +/- 31 units/ml (mean +/- S.D.) and 39 +/- 34 units/ml, respectively. The highest frequency of positive results (88%) was obtained in patients with auto-immune hypothyroidism (clinical diagnosis: Hashimoto's thyroiditis) followed by patients with Graves' disease (53%). With a cut-off point of 200 units/ml, a sensitivity of 96% was obtained for Hashimoto's thyroiditis and of 59% for Graves' disease with a specificity of 100% (50 cases). The new method (anti-TPO, Dynotest) was compared with three conventional methods (35 samples). The results for all measurements were in general agreement. In two cases the results were clearly discordant: one sample contained high anti-thyroglobulin antibody concentrations, the other was obtained from a patient with non-thyroidal illness. In both instances the 'classical' assays yielded false-positive results. Treatment of autoimmune hyperthyroidism resulted in a median decrease in anti-TPO levels of over 50% after reaching the euthyroid state (P < 0.05), whereas in persistent hyperthyroidism no consistent changes were observed. In autoimmune hypothyroidism a marked variability in anti-TPO levels was noted. Some patients showed a clear decrease in anti-TPO levels during T4 substitution whereas in others no consistent changes were observed.

Autoantibodies↗