2014
DOI: 10.1089/thy.2013.0142
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Differential Regulation of the Production of Reactive Oxygen Species in Th1 Cytokine–Treated Thyroid Cells

Abstract: The data presented here reinforce the idea that ROS, other than extracellular H2O2 produced by DUOX, are released from NOX2 after exposure of thyroid cells to Th1 cytokines. ROS/reactive nitrogen species act as important, but as further explained, not exclusive intracellular mediators of Th1 cytokine-induced effects in thyroid cells.

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Cited by 18 publications
(12 citation statements)
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“…The levels of IL1β in group II were significantly decreased (Ме 3.90 pg/mL; range: 2.35–42.24 pg/mL) in comparison with those observed in group I (Me 15.42 pg/mL; range: 5.80–38.20 pg/mL; p < 0.01). This finding is consistent with recent research data on the immune regulatory properties of IL2 aimed at the differentiation of regulatory T cells [16, 17]. The balance of IFNγ/IL10 in animal blood serum increased to 1.9 and 1.2 in the groups with hypothyroidism and thyrotoxicosis, respectively.…”
Section: Resultssupporting
confidence: 93%
“…The levels of IL1β in group II were significantly decreased (Ме 3.90 pg/mL; range: 2.35–42.24 pg/mL) in comparison with those observed in group I (Me 15.42 pg/mL; range: 5.80–38.20 pg/mL; p < 0.01). This finding is consistent with recent research data on the immune regulatory properties of IL2 aimed at the differentiation of regulatory T cells [16, 17]. The balance of IFNγ/IL10 in animal blood serum increased to 1.9 and 1.2 in the groups with hypothyroidism and thyrotoxicosis, respectively.…”
Section: Resultssupporting
confidence: 93%
“…Our study shows that NOX4 was increased in human thyroid cells treated with Th1 cytokines, as well as in HT thyroid samples, while NOX2 expression was not modified. This is in contrast to the results reported by Colin et al (2014) [10] and this could be explained by the fact that we used primary cultures of human thyroid cells rather than PCCL3 cell lines. Colin et al (2014) [10] analyzed the NOX2 protein level by immunohistochemistry on two HT patients without making the distinction between the different types of follicles.…”
Section: Discussioncontrasting
confidence: 82%
“…Moreover, Werion et al (2016) highlighted that a decrease in PPARγ, a well-known regulator of Cav-1 and also of the antioxidant catalase, is a key event in HT pathogenesis [9]. Colin et al (2014) proposed that ROS production induced by Th1 cytokines in thyroid cell lines results from NOX2 upregulation and, thus, superoxide overproduction [10]. They did not observe any modification of NOX4 expression in the PCCL3 cell lines and in the thyroid samples of two HT patients.…”
Section: Introductionmentioning
confidence: 98%
“…First, inflammation directly increases the level of hydrogen peroxide in thyroid epithelial cells, and second, it activates NOX enzyme in T and B lymphocytes, which increases ROS production (22,23). In fact, the Th1 cytokines (predominant in HT) are known to decrease DUOX and thus H 2 O 2 production but to increase NOX2 (without affecting NOX4) (24). Another reason for the determination of a low TAS level in the hypothyroidism group compared to other groups may be a decreased thyroid hormone level, because thyroid hormones are known to affect synthesis and bioactivity of antioxidant enzymes (25,26).…”
Section: European Journal Of Endocrinologymentioning
confidence: 99%