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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Mouse glucocorticoid-induced tumor necrosis factor receptor ligand is costimulatory for T cells
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Mouse glucocorticoid-induced tumor necrosis factor receptor ligand is costimulatory for T cells

机译:小鼠糖皮质激素诱导的肿瘤坏死因子受体配体可共同刺激T细胞

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摘要

Recently, agonist antibodies to glucocorticoid-induced tumor necrosis factor receptor (GITR) (tumor necrosis factor receptor super-family 18) have been shown to neutralize the suppressive activity of CD4~+CD25~+ regulatory T cells. It was anticipated that this would be the role of the physiological ligand. We have identified and expressed the gene for mouse GITR ligand and have confirmed that its interaction with GITR reverses suppression by CD4~+CD25~+ T cells. It also, however, provides a costimulatory signal for the antigen-driven proliferation of naive T cells and polarized T helper 1 and T helper 2 clones. RT-PCR and mAb staining revealed mouse GITR ligand expression in dendritic cells, macrophages, and B cells. Expression was controlled by the transcription factor NF-1 and potentially by alternative splicing of mRNA destabilization sequences.
机译:近来,已显示出针对糖皮质激素诱导的肿瘤坏死因子受体(GITR)(肿瘤坏死因子受体超家族18)的激动剂抗体可中和CD4〜+ CD25〜+调节性T细胞的抑制活性。预期这将是生理配体的作用。我们已经鉴定并表达了小鼠GITR配体的基因,并证实了其与GITR的相互作用逆转了CD4〜+ CD25〜+ T细胞的抑制作用。但是,它也为天然T细胞以及极化的T辅助1和T辅助2克隆的抗原驱动的增殖提供了共刺激信号。 RT-PCR和mAb染色显示树突状细胞,巨噬细胞和B细胞中的小鼠GITR配体表达。表达受转录因子NF-1的控制,并可能受mRNA不稳定序列的选择性剪接控制。

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