Background: Microvesicles (MVs) are emerging as important contributors to the development of inflammatory and autoimmune diseases. MVs can mediate immune modulation carrying genetic information, including microRNAs that can be transferred between cells. Design:Wedetermined the plasma levels of annexin-V MVs derived from different immune cells and platelets in patients with autoimmune thyroid diseases (AITDs) and in healthy controls. T lymphocyte polarization assays were performed in the presence of MVs to evaluate their effect in T regulatory and T helper 17 cells differentiation. microRNA content into plasma MVs and their corresponding mRNA targets were evaluated by RT-PCR. Results: The percentage of platelet-derived MVs (CD41a ) was significantly increased in plasma samples from AITD patients compared with healthy controls. In contrast, patients with AITD showeda lower percentage of leukocyteandendothelial cell-derivedMVscompared with controls. In addition, functional assays showed that MVs from AITD patients inhibited the in vitro differentiation of Foxp3 T regulatory cells (11.35%25 vs 4.40%25, P = .01) and induced the expression of interferon-γ by CD4 lymphocytes (10.91%25 vs 13.99%25, P = .01) as well as the differentiation of T helper 17 pathogenic (IL-17 interferon-γ ) cells (1.98%25 vs 5.13%25, P = .03). Furthermore, in AITD patients, whereas miR-146a and miR-155 were increased in circulating MVs, their targets IL-8 and SMAD4 were decreased in peripheral blood mononuclear cells. Conclusions: Our data indicate that circulating MVs seem to have a relevant role in the modulation of the inflammatory response observed in AITD. Copyright © 2015 by the Endocrine Society.
Background: Microvesicles (MVs) are emerging as important contributors to the development of inflammatory and autoimmune diseases. MVs can mediate immune modulation carrying genetic information, including microRNAs that can be transferred between cells. Design:Wedetermined the plasma levels of annexin-V%2bMVs derived from different immune cells and platelets in patients with autoimmune thyroid diseases (AITDs) and in healthy controls. T lymphocyte polarization assays were performed in the presence of MVs to evaluate their effect in T regulatory and T helper 17 cells differentiation. microRNA content into plasma MVs and their corresponding mRNA targets were evaluated by RT-PCR. Results: The percentage of platelet-derived MVs (CD41a%2b) was significantly increased in plasma samples from AITD patients compared with healthy controls. In contrast, patients with AITD showeda lower percentage of leukocyteandendothelial cell-derivedMVscompared with controls. In addition, functional assays showed that MVs from AITD patients inhibited the in vitro differentiation of Foxp3%2b T regulatory cells (11.35%25 vs 4.40%25, P = .01) and induced the expression of interferon-γ by CD4%2b lymphocytes (10.91%25 vs 13.99%25, P = .01) as well as the differentiation of T helper 17 pathogenic (IL-17%2binterferon-γ%2b) cells (1.98%25 vs 5.13%25, P = .03). Furthermore, in AITD patients, whereas miR-146a and miR-155 were increased in circulating MVs, their targets IL-8 and SMAD4 were decreased in peripheral blood mononuclear cells. Conclusions: Our data indicate that circulating MVs seem to have a relevant role in the modulation of the inflammatory response observed in AITD. Copyright © 2015 by the Endocrine Society.
gamma interferon; interleukin 8; lipocortin 5; messenger RNA; microRNA; microRNA 146a; microRNA 155; Smad4 protein; IL8 protein, human; interleukin 8; messenger RNA; microRNA; MIRN146 microRNA, human; MIRN155 microRNA, human; Smad4 protein; SMAD4 protein, human; apoptosis; Article; CD4 T lymphocyte; controlled study; endothelium cell; flow cytometry; Graves disease; Hashimoto disease; human; human cell; immunoblotting; immunocompetent cell; in vitro study; leukocyte; lymphocyte differentiation; major clinical study; membrane microparticle; peripheral blood mononuclear cell; priority journal; protein blood level; protein expression; regulatory T lymphocyte; reverse transcription polymerase chain reaction; Th17 cell; thrombocyte; autoimmune thyroiditis; blood; cell differentiation; chemistry; cytoplasm vesicle; metabolism; pathology; polymerase chain reaction; regulatory T lymphocyte; Th17 cell; Apoptosis; Blood Platelets; CD4-Positive T-Lymphocytes; Cell Differentiation; Cytoplasmic Vesicles; Flow Cytometry; Humans; Interleukin-8; MicroRNAs; Polymerase Chain Reaction; RNA, Messenger; Smad4 Protein; T-Lymphocytes, Regulatory; Th17 Cells; Thyroiditis, Autoimmune
Circulating microvesicles regulate treg and Th17 differentiation in human autoimmune thyroid disorders
gamma interferon; interleukin 8; lipocortin 5; messenger RNA; microRNA; microRNA 146a; microRNA 155; Smad4 protein; IL8 protein, human; interleukin 8; messenger RNA; microRNA; MIRN146 microRNA, human; MIRN155 microRNA, human; Smad4 protein; SMAD4 protein, human; apoptosis; Article; CD4+ T lymphocyte; controlled study; endothelium cell; flow cytometry; Graves disease; Hashimoto disease; human; human cell; immunoblotting; immunocompetent cell; in vitro study; leukocyte; lymphocyte differentiation; major clinical study; membrane microparticle; peripheral blood mononuclear cell; priority journal; protein blood level; protein expression; regulatory T lymphocyte; reverse transcription polymerase chain reaction; Th17 cell; thrombocyte; autoimmune thyroiditis; blood; cell differentiation; chemistry; cytoplasm vesicle; metabolism; pathology; polymerase chain reaction; regulatory T lymphocyte; Th17 cell; Apoptosis; Blood Platelets; CD4-Positive T-Lymphocytes; Cell Differentiation; Cytoplasmic Vesicles; Flow Cytometry; Humans; Interleukin-8; MicroRNAs; Polymerase Chain Reaction; RNA, Messenger; Smad4 Protein; T-Lymphocytes, Regulatory; Th17 Cells; Thyroiditis, Autoimmune
gamma interferon, 82115-62-6; interleukin 8, 114308-91-7; lipocortin 5, 111237-10-6; Smad4 protein, 282562-18-9; IL8 protein, human; Interleukin-8; MicroRNAs; MIRN146 microRNA, human; MIRN155 microRNA, human; RNA, Messenger; Smad4 Protein; SMAD4 protein, human
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Journal of Clinical Endocrinology and Metabolism
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