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自身免疫性甲状腺疾病患儿 CD4+CD25(high) 和 CD4+FoxP3 的比例较低,但 CD4+CD25+CD127(low)FoxP3+T 细胞水平没有变化。

Lower proportions of CD4+CD25(high) and CD4+FoxP3, but not CD4+CD25+CD127(low) FoxP3+ T cell levels in children with autoimmune thyroid diseases.

机构信息

Department of Pediatrics Endocrinology, Diabetology with Cardiology Division, Medical University of Bialystok, Poland.

出版信息

Autoimmunity. 2013 May;46(3):222-30. doi: 10.3109/08916934.2012.751981. Epub 2013 Jan 22.

Abstract

The essence of autoimmune thyroid disease (AITD) is loss of tolerance of own tissues caused by malfunction of T lymphocytes, which affects the production of antibodies reacting with particular cell structures and tissues. Foxp3(+) regulatory T cells (Tregs) take part in the regulation of immune response and play a leading role in developing immune tolerance through active suppression. The aim of the study was to estimate the expression of CD4+CD25(high), CD4+CD25+CD127(low)FoxP3(+) and CD4+ FoxP3 T cells in patients with Graves' disease (GD) (n = 24, median age 15.5 years), in patients with Hashimoto's thyroiditis (HT) (n = 30, median age 15 years) in comparison with sex- and age-matched healthy control subjects (n = 30, median age 15 years). Polychromatic flow cytometry using a FACSCalibur (BD Biosciences) cytometer was applied to delineate T regulatory cell populations. In untreated patients with Graves' disease and HT we observed a significant decrease in CD4+FoxP3 (p < 0.001, p < 0.01) and CD4+CD25(high) (p < 0.016, p < 0.048) T lymphocytes as compared to the healthy control subjects. After 6-12 months of L-thyroxine therapy in HT cases these phenotypes of Tregs were normalized, yet no such changes were observed during GD therapy. The analysis of CD4+CD25+CD127(low)FoxP3+ T cells in the peripheral blood revealed comparable percentages of these cells in patients with thyroid autoimmune diseases to the controls. We conclude that the reduction number of Tregs with CD4+CD25(high) and CD4+FoxP3 phenotype suggests their role in initiation and development of autoimmune process in thyroid disorders.

摘要

自身免疫性甲状腺疾病(AITD)的本质是 T 淋巴细胞功能障碍导致自身组织的耐受性丧失,这会影响与特定细胞结构和组织发生反应的抗体的产生。Foxp3(+)调节性 T 细胞(Tregs)参与免疫反应的调节,通过主动抑制发挥主导作用,从而形成免疫耐受。本研究旨在评估 Graves 病(GD)(n = 24,中位年龄 15.5 岁)、桥本甲状腺炎(HT)(n = 30,中位年龄 15 岁)患者与年龄、性别相匹配的健康对照组(n = 30,中位年龄 15 岁)之间 CD4+CD25(high)、CD4+CD25+CD127(low)FoxP3(+)和 CD4+FoxP3 T 细胞的表达。使用 FACSCalibur(BD Biosciences)流式细胞仪进行多色流式细胞术,以描绘 T 调节细胞群。在未经治疗的 GD 和 HT 患者中,与健康对照组相比,我们观察到 CD4+FoxP3(p < 0.001,p < 0.01)和 CD4+CD25(high)(p < 0.016,p < 0.048)T 淋巴细胞显著减少。在 HT 病例中,经过 6-12 个月的 L-甲状腺素治疗后,这些 Treg 表型恢复正常,但在 GD 治疗过程中未观察到这种变化。在外周血中分析 CD4+CD25+CD127(low)FoxP3+T 细胞,发现这些细胞在甲状腺自身免疫性疾病患者与对照组中的比例相当。我们得出结论,具有 CD4+CD25(high)和 CD4+FoxP3 表型的 Treg 数量减少表明其在甲状腺疾病自身免疫过程的启动和发展中发挥作用。

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