Association of IFNG gene methylation in peripheral blood cells with the development and prognosis of autoimmune thyroid diseases

Cytokine ◽  
2019 ◽  
Vol 123 ◽  
pp. 154770 ◽  
Author(s):  
Hidemi Hashimoto ◽  
Mikio Watanabe ◽  
Naoya Inoue ◽  
Nachi Hirai ◽  
Emi Haga ◽  
...  
Autoimmunity ◽  
2019 ◽  
Vol 52 (7-8) ◽  
pp. 251-255 ◽  
Author(s):  
Nachi Hirai ◽  
Mikio Watanabe ◽  
Naoya Inoue ◽  
Riku Kinoshita ◽  
Hiroki Ohtani ◽  
...  

2019 ◽  
Vol 49 (1-2) ◽  
pp. 191-203 ◽  
Author(s):  
Ayano Watanabe ◽  
Naoya Inoue ◽  
Mikio Watanabe ◽  
Mayu Yamamoto ◽  
Haruka Ozaki ◽  
...  

2020 ◽  
Vol 19 (5) ◽  
pp. 774-792 ◽  
Author(s):  
Tiphaine C. Martin ◽  
Mirna Šimurina ◽  
Marta Ząbczyńska ◽  
Marina Martinic Kavur ◽  
Magdalena Rydlewska ◽  
...  

Autoimmune thyroid diseases (AITD) are the most common group of autoimmune diseases, associated with lymphocyte infiltration and the production of thyroid autoantibodies, like thyroid peroxidase antibodies (TPOAb), in the thyroid gland. Immunoglobulins and cell-surface receptors are glycoproteins with distinctive glycosylation patterns that play a structural role in maintaining and modulating their functions. We investigated associations of total circulating IgG and peripheral blood mononuclear cells glycosylation with AITD and the influence of genetic background in a case-control study with several independent cohorts and over 3,000 individuals in total. The study revealed an inverse association of IgG core fucosylation with TPOAb and AITD, as well as decreased peripheral blood mononuclear cells antennary α1,2 fucosylation in AITD, but no shared genetic variance between AITD and glycosylation. These data suggest that the decreased level of IgG core fucosylation is a risk factor for AITD that promotes antibody-dependent cell-mediated cytotoxicity previously associated with TPOAb levels.


2016 ◽  
Vol 73 (3) ◽  
pp. 465-474 ◽  
Author(s):  
Rodrigo San-Cristobal ◽  
Santiago Navas-Carretero ◽  
Fermín I. Milagro ◽  
J. Ignacio Riezu-Boj ◽  
Elizabeth Guruceaga ◽  
...  

2018 ◽  
Vol 103 (3) ◽  
pp. 1139-1150 ◽  
Author(s):  
Rebeca Martínez-Hernández ◽  
Miguel Sampedro-Núñez ◽  
Ana Serrano-Somavilla ◽  
Ana M Ramos-Leví ◽  
Hortensia de la Fuente ◽  
...  

Abstract Context Circulating microRNAs (miRNAs) are emerging as an interesting research area because of their potential role as novel biomarkers and therapeutic targets. Their involvement in autoimmune thyroid diseases (AITDs) has not been fully explored. Objective To compare the expression profile of miRNAs in thyroid tissue from patients with AITD and controls, using next-generation sequencing, further validated our findings in thyroid and serum samples. Design Twenty fresh-frozen thyroid tissues (15 from patients with AITD and 5 from controls) were used for miRNA next-generation sequencing. Thirty-six thyroid samples were recruited for the qRT-PCR validation test and 58 serum samples for further validation in peripheral blood. Results Expression of several miRNAs that had been previously associated with relevant immunological functions was significantly dysregulated. Specifically, eight differentially expressed miRNAs (miR-21-5p, miR-142-3p, miR-146a-5p, miR-146b-5p, miR-155-5p, miR-338-5p, miR-342-5p, and miR-766-3p) were confirmed using qRT-PCR in thyroid samples, and three had the same behavior in tissue and serum samples (miR-21-5p, miR-142-3p, and miR-146a-5p). Furthermore, when the expression of these miRNAs was assessed together with five additional ones previously related to AITD in peripheral blood, the expression of five (miR-Let7d-5p, miR-21-5p, miR-96-5p, miR-142-3p, and miR-301a-3p) was significantly expressed in AITD and, in patients with Graves disease (GD), was correlated with a higher severity of disease, including active ophthalmopathy, goiter, higher antibody titers, and/or higher recurrence rates. Conclusions The present findings identify a serum five-signature miRNA that could be an independent risk factor for developing AITD and a predisposition of a worse clinical picture in patients with GD.


1987 ◽  
Vol 58 (03) ◽  
pp. 936-942 ◽  
Author(s):  
Lindsey A Miles ◽  
Edward F Plow

SummaryGlu-plasminogen binds to platelets; the monocytoid line, U937, and the human fetal fibroblast line, GM1380 bind both plasminogen and its activator, urokinase. This study assesses the interaction of these fibrinolytic proteins with circulating human blood cells. Plasminogen bound minimally to red cells but bound saturably and reversibly to monocytes, granulocytes and lymphocytes with apparent Kd values of 0.9-1.4 μM. The interactions were of high capacity with 1.6 to 49 × 105 sites/cell and involved the lysine binding sites of plasminogen. Both T cells and non-rosetting lymphocytes and two B cell lines saturably bound plasminogen. Urokinase bound saturably to gianulocytes, monocytes, non-rosetting lymphocytes and a B cell line, but minimally to T cells, platelets and red cells. Therefore, plasminogen binding sites of high capacity, of similar affinities, and with common recognition specificities are expressed by many peripheral blood cells. Urokinase receptors are also widely distributed, but less so than plasminogen binding sites. The binding ol plasminogen and/ or urokinase to these cells may lead to generation of cell- associated proteolytic activity which contributes to a variety of cellular functions.


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