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CD69 antigen; interleukin 10; interleukin 2 receptor alpha; transcription factor FOXP3; transforming growth factor beta; tumor necrosis factor receptor; article; autoimmune disease; autoimmune thyroid disease; cell proliferation; clinical article; controlled study; flow cytometry; human; human cell; human tissue; immunohistochemistry; in vitro study; peripheral blood mononuclear cell; polymerase chain reaction; priority journal; regulatory T lymphocyte; thyroid disease; Animalia
Regulatory T cells in human autoimmune thyroid disease
Context: T regulatory cells have a key role in the pathogenesis of autoimmune diseases in different animal models. However, less information is available regarding these cells in human autoimmune thyroid diseases (AITD). Objective: The objective of the study was to analyze different regulatory T cell subsets in patients with AITD. Design: We studied by flow cytometry and immunohistochemistry different T regulatory cell subsets in peripheral blood mononuclear cells (PBMCs) and thyroid cell infiltrates from 20 patients with AITD. In addition, the function of TREG lymphocytes was assessed by cell proliferation assays. Finally, TGF-β mRNA in thyroid tissue and its in vitro synthesis by thyroid mononuclear cells (TMCs) was determined by RNase protection assay and quantitative PCR. Results: PBMCs from AITD patients showed an increased percent of CD4 lymphocytes expressing glucocorticoid-induced TNF receptor (GITR), Foxp3, IL-10, TGF-β, and CD69 as well as CD69 CD25 bright, CD69 TGF-β, and CD69 IL-10 cells, compared with controls. TMCs from these patients showed an increased proportion of CD4 GITR , CD4 CD69 , and CD69 cells expressing CD25bright, GITR, and Foxp3, compared with autologous PBMCs. Furthermore, a prominent infiltration of thyroid tissue by CD69 , CD25 , and GITR cells, with moderate levels of Foxp3 lymphocytes, was observed. The suppressive function of peripheral blood T REG cells was defective in AITD patients. Finally, increased levels of TGF-β mRNA were found in thyroid tissue, and thyroid cell infiltrates synthesized in vitro significant levels of TGF-β upon stimulation through CD69. Conclusions: Although T regulatory cells are abundant in inflamed thyroid tissue, they are apparently unable, in most cases, to down-modulate the autoimmune response and the tissue damage seen in AITD. Copyright © 2006 by The Endocrine Society.
tumor necrosis factor receptor, 129203-93-6, 184595-01-5
Context: T regulatory cells have a key role in the pathogenesis of autoimmune diseases in different animal models. However, less information is available regarding these cells in human autoimmune thyroid diseases (AITD). Objective: The objective of the study was to analyze different regulatory T cell subsets in patients with AITD. Design: We studied by flow cytometry and immunohistochemistry different T regulatory cell subsets in peripheral blood mononuclear cells (PBMCs) and thyroid cell infiltrates from 20 patients with AITD. In addition, the function of TREG lymphocytes was assessed by cell proliferation assays. Finally, TGF-β mRNA in thyroid tissue and its in vitro synthesis by thyroid mononuclear cells (TMCs) was determined by RNase protection assay and quantitative PCR. Results: PBMCs from AITD patients showed an increased percent of CD4%2b lymphocytes expressing glucocorticoid-induced TNF receptor (GITR), Foxp3, IL-10, TGF-β, and CD69 as well as CD69%2bCD25 bright, CD69%2bTGF-β, and CD69%2bIL-10%2b cells, compared with controls. TMCs from these patients showed an increased proportion of CD4%2bGITR%2b, CD4%2bCD69%2b, and CD69%2b cells expressing CD25bright, GITR, and Foxp3, compared with autologous PBMCs. Furthermore, a prominent infiltration of thyroid tissue by CD69%2b, CD25%2b, and GITR%2b cells, with moderate levels of Foxp3%2b lymphocytes, was observed. The suppressive function of peripheral blood T REG cells was defective in AITD patients. Finally, increased levels of TGF-β mRNA were found in thyroid tissue, and thyroid cell infiltrates synthesized in vitro significant levels of TGF-β upon stimulation through CD69. Conclusions: Although T regulatory cells are abundant in inflamed thyroid tissue, they are apparently unable, in most cases, to down-modulate the autoimmune response and the tissue damage seen in AITD. Copyright © 2006 by The Endocrine Society.
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Journal of Clinical Endocrinology and Metabolism
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