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1.发明申请公开(公告)号：US20110034532A1
公开(公告)日：2011-02-10
申请号：US12792585
申请日：2010-06-02
申请人： QI-JING LI , CHANG-ZHENG CHEN , MARK M. DAVIS , JACQUELINE CHAU
发明人： QI-JING LI , CHANG-ZHENG CHEN , MARK M. DAVIS , JACQUELINE CHAU
CPC分类号： C12N15/113 , A61K39/00 , A61K2039/57 , C12N2310/11 , C12N2310/113 , C12N2310/141 , C12N2310/315 , C12N2310/321 , C12N2310/3515 , G01N33/5041 , G01N33/505 , G01N2500/02 , G01N2800/24 , C12N2310/3521
摘要： MicroRNAs (miRNAs) are a diverse and abundant class of ˜22-nucleotide (nt) endogenous regulatory RNAs that play a variety of roles in animal cells by controlling gene expression at the posttranscriptional level. Increased miR-181a expression in mature T cells is shown to cause a marked increase in T cell activation and augments T cell sensitivity to peptide antigens. Moreover, T cell blasts with higher miR-181a expression become reactive to antagonists. The effects of miR-181a on antigen discrimination are in part achieved by dampening the expression of multiple negative regulators in the T cell receptor (TCR) signaling pathway, including PTPN22 and the dual specificity phosphatases DUSP5 and DUSP6. This results in a reduction in the TCR signaling threshold, thus quantitatively and qualitatively enhancing T cell sensitivity to antigens.
摘要翻译： 微RNA（miRNA）是一种多样且丰富的〜22核苷酸（nt）内源性调控RNA，通过控制转录后水平的基因表达，在动物细胞中发挥各种作用。 在成熟T细胞中增加的miR-181a表达显示引起T细胞活化的显着增加并增加T细胞对肽抗原的敏感性。 此外，具有较高miR-181a表达的T细胞爆发成为对拮抗剂的反应性。 miR-181a对抗原鉴别的影响部分通过抑制T细胞受体（TCR）信号通路中多种负调节因子的表达，包括PTPN22和双特异性磷酸酶DUSP5和DUSP6来实现。 这导致TCR信号阈值的降低，从而定量和定性地增强T细胞对抗原的敏感性。
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2.发明授权公开(公告)号：US08741860B2
公开(公告)日：2014-06-03
申请号：US12792585
申请日：2010-06-02
申请人： Qi-Jing Li , Chang-Zheng Chen , Mark M. Davis , Jacqueline Chau
发明人： Qi-Jing Li , Chang-Zheng Chen , Mark M. Davis , Jacqueline Chau
CPC分类号： C12N15/113 , A61K39/00 , A61K2039/57 , C12N2310/11 , C12N2310/113 , C12N2310/141 , C12N2310/315 , C12N2310/321 , C12N2310/3515 , G01N33/5041 , G01N33/505 , G01N2500/02 , G01N2800/24 , C12N2310/3521
摘要： MicroRNAs (miRNAs) are a diverse and abundant class of ˜22-nucleotide (nt) endogenous regulatory RNAs that play a variety of roles in animal cells by controlling gene expression at the posttranscriptional level. Increased miR-181a expression in mature T cells is shown to cause a marked increase in T cell activation and augments T cell sensitivity to peptide antigens. Moreover, T cell blasts with higher miR-181a expression become reactive to antagonists. The effects of miR-181a on antigen discrimination are in part achieved by dampening the expression of multiple negative regulators in the T cell receptor (TCR) signaling pathway, including PTPN22 and the dual specificity phosphatases DUSP5 and DUSP6. This results in a reduction in the TCR signaling threshold, thus quantitatively and qualitatively enhancing T cell sensitivity to antigens.
摘要翻译： 微RNA（miRNA）是一种多样且丰富的〜22核苷酸（nt）内源性调控RNA，通过控制转录后水平的基因表达，在动物细胞中发挥各种作用。 在成熟T细胞中增加的miR-181a表达显示引起T细胞活化的显着增加并增加T细胞对肽抗原的敏感性。 此外，具有较高miR-181a表达的T细胞爆发成为对拮抗剂的反应性。 miR-181a对抗原鉴别的影响部分通过抑制T细胞受体（TCR）信号通路中多种负调节因子的表达，包括PTPN22和双重特异性磷酸酶DUSP5和DUSP6来实现。 这导致TCR信号阈值的降低，从而定量和定性地增强T细胞对抗原的敏感性。
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3.发明申请公开(公告)号：US20080200416A1
公开(公告)日：2008-08-21
申请号：US11977506
申请日：2007-10-24
申请人： Qi-Jing Li , Chang-Zheng Chen , Mark M. Davis , Jacqueline Chau
发明人： Qi-Jing Li , Chang-Zheng Chen , Mark M. Davis , Jacqueline Chau
CPC分类号： C12N15/113 , A61K39/00 , A61K2039/57 , C12N2310/11 , C12N2310/113 , C12N2310/141 , C12N2310/315 , C12N2310/321 , C12N2310/3515 , G01N33/5041 , G01N33/505 , G01N2500/02 , G01N2800/24 , C12N2310/3521
摘要： MicroRNAs (miRNAs) are a diverse and abundant class of ˜22-nucleotide (nt) endogenous regulatory RNAs that play a variety of roles in animal cells by controlling gene expression at the posttranscriptional level. Increased miR-181a expression in mature T cells is shown to cause a marked increase in T cell activation and augments T cell sensitivity to peptide antigens. Moreover, T cell blasts with higher miR-181a expression become reactive to antagonists. The effects of miR-181a on antigen discrimination are in part achieved by dampening the expression of multiple negative regulators in the T cell receptor (TCR) signaling pathway, including PTPN22 and the dual specificity phosphatases DUSP5 and DUSP6. This results in a reduction in the TCR signaling threshold, thus quantitatively and qualitatively enhancing T cell sensitivity to antigens.
摘要翻译： 微RNA（miRNA）是一种多样且丰富的〜22个核苷酸（nt）内源性调控RNA，通过控制转录后水平的基因表达，在动物细胞中发挥各种作用。 在成熟T细胞中增加的miR-181a表达显示引起T细胞活化的显着增加并增加T细胞对肽抗原的敏感性。 此外，具有较高miR-181a表达的T细胞爆发成为对拮抗剂的反应性。 miR-181a对抗原鉴别的影响部分通过抑制T细胞受体（TCR）信号通路中多种负调节因子的表达，包括PTPN22和双特异性磷酸酶DUSP5和DUSP6来实现。 这导致TCR信号阈值的降低，从而定量和定性地增强T细胞对抗原的敏感性。
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4.发明授权公开(公告)号：US07803784B2
公开(公告)日：2010-09-28
申请号：US11977506
申请日：2007-10-24
申请人： Qi-Jing Li , Chang-Zheng Chen , Mark M. Davis , Jacqueline Chau
发明人： Qi-Jing Li , Chang-Zheng Chen , Mark M. Davis , Jacqueline Chau
CPC分类号： C12N15/113 , A61K39/00 , A61K2039/57 , C12N2310/11 , C12N2310/113 , C12N2310/141 , C12N2310/315 , C12N2310/321 , C12N2310/3515 , G01N33/5041 , G01N33/505 , G01N2500/02 , G01N2800/24 , C12N2310/3521
摘要： MicroRNAs (miRNAs) are a diverse and abundant class of ˜22-nucleotide (nt) endogenous regulatory RNAs that play a variety of roles in animal cells by controlling gene expression at the posttranscriptional level. Increased miR-181a expression in mature T cells is shown to cause a marked increase in T cell activation and augments T cell sensitivity to peptide antigens. Moreover, T cell blasts with higher miR-181a expression become reactive to antagonists. The effects of miR-181a on antigen discrimination are in part achieved by dampening the expression of multiple negative regulators in the T cell receptor (TCR) signaling pathway, including PTPN22 and the dual specificity phosphatases DUSP5 and DUSP6. This results in a reduction in the TCR signaling threshold, thus quantitatively and qualitatively enhancing T cell sensitivity to antigens.
摘要翻译： 微RNA（miRNA）是一种多样且丰富的〜22核苷酸（nt）内源性调控RNA，通过控制转录后水平的基因表达，在动物细胞中发挥各种作用。 在成熟T细胞中增加的miR-181a表达显示引起T细胞活化的显着增加并增加T细胞对肽抗原的敏感性。 此外，具有较高miR-181a表达的T细胞爆发成为对拮抗剂的反应性。 miR-181a对抗原鉴别的影响部分通过抑制T细胞受体（TCR）信号通路中多种负调节因子的表达，包括PTPN22和双特异性磷酸酶DUSP5和DUSP6来实现。 这导致TCR信号阈值的降低，从而定量和定性地增强T细胞对抗原的敏感性。
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