细胞凋亡
甲状腺炎
甲状腺
Fas配体
内分泌学
内科学
淋巴细胞浸润
细胞生长
癌症研究
医学
生物
程序性细胞死亡
生物化学
作者
Jessica Castro de Vasconcelos,Icleia Barreto de Siqueira,Frederico Fernandes Ribeiro Maia,Maria Cândida Ribeiro Parisi,Denise Engelbrecht Zantut‐Wittmann
标识
DOI:10.1016/j.mce.2021.111421
摘要
Cell destruction in Hashimoto's thyroiditis (HT) involves autoantibodies and cytotoxic T lymphocytes. Thyrocytes maintenance occurs by pro-apoptotic, anti-apoptotic and cell proliferation balance. To characterize factors related to the mechanisms of apoptosis and cell proliferation in thyroid cells and intrathyroid lymphocytic infiltrate in HT. We assessed lymphocytic infiltrate and thyroid cells from HT and normal thyroid by immunohistochemical analysis of cell proliferation (Ki-67), antiproliferation (p27Kip1), pro-apoptosis (Fas, Fas-ligand, BID) and anti-apoptosis (MCL-1, BCL2) markers. Lymphocytic infiltrate presented BCL2 and MCL-1 higher expression, Ki-67 and p27kip1 balance. Thyrocytes exhibited Fas and FasL balance, higher BID expression; MCL-1, BCL-2, Ki-67 similar to the normal thyroid. T4 and higher lymphocytes BID expression were associated. In lymphocytic infiltrate predominated anti-apoptosis in relation to pro-apoptosis except for BID. Thyrocytes presented pro-apoptosis and anti-apoptosis balance and cell proliferation similar to normal thyroid. T4-associated BID expression in HT lymphocytes suggests the influence of thyroid hormone as a signal to up-regulate the BID pro-apoptotic protein and thus increase lymphocytic apoptosis rates.
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