scholarly journals Depletion of Regulatory T Cells in Visceral Adipose Tissues Contributes to Insulin Resistance in Hashimoto's Thyroiditis

2018 ◽  
Vol 9 ◽  
Author(s):  
Min Yang ◽  
Li Su ◽  
Qin Tao ◽  
Chenxi Zhang ◽  
Yueyue Wu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
T Cells ◽  
Regulatory T Cells ◽  
Hashimoto’S Thyroiditis ◽  
Hashimoto's Thyroiditis ◽  
Adipose Tissues ◽  
Visceral Adipose

Increased circulating follicular regulatory T cells in Hashimoto’s thyroiditis

Autoimmunity ◽  
2018 ◽  
Vol 51 (7) ◽  
pp. 345-351 ◽  
Author(s):  
Jiwei Zhao ◽  
Yanxia Chen ◽  
Zhenyao Xu ◽  
Wei Yang ◽  
Zhongliang Zhu ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Hashimoto’S Thyroiditis ◽  
Hashimoto's Thyroiditis

Pathology

2020 ◽  
pp. 16-24
Keyword(s):  
T Cells ◽  
Hashimoto’S Thyroiditis ◽  
Plasma Cells ◽  
Lymphocytic Infiltration ◽  
Lymphoid Cells ◽  
Hashimoto's Thyroiditis ◽  
Gamma Delta T Cells ◽  
Cellular Infiltration ◽  
Pyramidal Lobe ◽  
Grade Iii

Grossly, thyroid enlargement in Hashimoto's thyroiditis (HT) is generally symmetrical, often with a characteristic conspicuous pyramidal lobe. The tissue involved by HT is pinkish-tan to frankly yellowish in color and tends to have a rubbery firmness. There is no necrosis or calcification. The capsule is intact and non-adherent to peri-thyroid structures. Microscopically, there is a diffuse process consisting of a combination of epithelial cell destruction, lymphoid cellular infiltration, and fibrosis. Lymphocytes are predominantly T-cells and plasma cells. Most infiltrating T-cells have α/β T-cell receptors. Gamma/delta T-cells are rare. Hashimoto's thyroiditis has been graded based on lymphocytic infiltration seen on cytology, into Grades 0-III, where Grade 0 means no lymphoid cells and Grade III severe lymphoid cell infiltration. Deposits of dense material representing IgG are found along the basement membrane on electron microscopy. This chapter explores the pathology of Hashimoto's disease.

scholarly journals Dietary glycemic index and dietary glycemic load is associated with apelin gene expression in visceral and subcutaneous adipose tissues of adults

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Emad Yuzbashian ◽  
Golaleh Asghari ◽  
Maryam Aghayan ◽  
Mehdi Hedayati ◽  
Maryam Zarkesh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Glycemic Index ◽  
Glycemic Load ◽  
Carbohydrate Intake ◽  
Model Assessment ◽  
Total Carbohydrate ◽  
Adipose Tissues ◽  
Visceral Adipose ◽  
Subcutaneous Adipose

Abstract Background Apelin, as an adipokine, plays an important role in the pathogenesis of insulin resistance and type 2 diabetes. This study aimed to determine whether the quality and quantity of dietary carbohydrates were associated with apelin gene expression in subcutaneous and visceral adipose tissues. Methods In this cross-sectional study, 102 adults who underwent minor abdominal surgery were selected. Approximately 100 mg of subcutaneous and visceral adipose tissues were collected during the surgery to measure apelin gene expression. Anthropometric measurment, blood samples, and dietary intakes were collected before surgery. The dietary carbohydrate intake, glycemic index (GI), and glycemic load (GL) were determined. Results The average apelin concentration was 269.6 ± 98.5(pg/mL), and 16.3% of participants were insulin resistant. There was a correlation between insulin (p-value = 0.043), Homeostatic Model Assessment for Insulin Resistance (HOMA-IR)(p-value = 0.045) and apelin gene expression in visceral adipose tissue. There was a positive association of apelin gene expression with dietary GI and GL after adjustment for age, sex, and waist circumference in visceral and subcutaneous adipose tissues(p < 0.05). Apelin gene expression in visceral(p = 0.002) and subcutaneous(p = 0.003) adipose tissues was directly associated with foods with a higher GI. There was no association between total carbohydrate intake and apelin gene expression in both visceral and subcutaneous adipose tissues. Conclusions Dietary GI and GL, not total carbohydrate intake, were positively associated with apelin gene expression in both visceral and subcutaneous adipose tissues. Future studies are warranted to illustrate the chronic and acute effect of carbohydrate quality on apelin homeostasis.

scholarly journals The Expression of T Cell FOXP3 and T-Bet Is Upregulated in Severe but Not Euthyroid Hashimoto’s Thyroiditis

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Stana Tokić ◽  
Mario Štefanić ◽  
Ljubica Glavaš-Obrovac ◽  
Sonja Jaman ◽  
Eva Novosadová ◽  
...  
Keyword(s):  
T Cells ◽  
Mrna Expression ◽  
Hashimoto’S Thyroiditis ◽  
Hormone Replacement ◽  
Study Groups ◽  
Hashimoto's Thyroiditis ◽  
Foxp3 Mrna ◽  
Expression Levels ◽  
Treg Subset ◽  
Mrna Expression Levels

Hashimoto’s thyroiditis (HT) is an organ-specific autoimmune disorder characterized by progressive thyroid failure. Th1 and Treg subset of CD4+ cells have been implicated in the pathogenesis; however, less is known about their respective roles across the spectrum of HT clinical presentations. To shed more light on CD4+ subsets role in HT, we investigated the mRNA expression levels of several Th1/Treg-associated transcription factors (T-bet/ETS1, HIF1α/BLIMP1/FOXP3) in peripheral blood T cells of 10 hypothyroid, untreated HT patients, 10 hypothyroid patients undergoing hormone replacement therapy, 12 euthyroid HT subjects, and 11 healthy controls by the qRT-PCR. Compared to euthyroid HT patients and controls, both hypothyroid (2.34-fold difference versus controls, P<0.01) and thyroxine-supplemented patients (2.5-fold, P<0.001) showed an increased FOXP3 mRNA expression in T cells. Similarly, mRNA expression levels of T-bet were upregulated in severely affected but not in euthyroid HT subjects (2.37-fold and 3.2-fold, hypothyroid and thyroxine-supplemented HT patients versus controls, resp., P<0.01). By contrast, no differences in mRNA expression levels of ETS1, BLIMP1, and HIF1α were observed across the study groups. In summary, severe but not euthyroid HT was associated with robust upregulation of T-bet and FOXP3 mRNA in peripheral T cells, independent of the thyroid hormone status but proportional to disease activity.

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