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Williams ES Stap J Essers J Ponnaiya B Luijsterburg MS Krawczyk PM Ullrich RL Aten JA Bailey SM 《Nature genetics》2007,39(6):696-8; author reply 698-9
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S.维雅克 《国外科技新书评介》2006,(9):10-11
2003年9月在斯洛文尼亚举行了“第十一届电子工程中的电磁场国际会议(ISEF’03)”,本书有选择性地收集了此次会议上的部分论文。ISEF的传统是包括广泛的计算和应用电磁学的范围,并促进理论与实际的结合,因此,大部分论文来自工程问题。 相似文献
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Negative regulation of lymphocyte activation and autoimmunity by the molecular adaptor Cbl-b 总被引:26,自引:0,他引:26
Bachmaier K Krawczyk C Kozieradzki I Kong YY Sasaki T Oliveira-dos-Santos A Mariathasan S Bouchard D Wakeham A Itie A Le J Ohashi PS Sarosi I Nishina H Lipkowitz S Penninger JM 《Nature》2000,403(6766):211-216
The signalling thresholds of antigen receptors and co-stimulatory receptors determine immunity or tolerance to self molecules. Changes in co-stimulatory pathways can lead to enhanced activation of lymphocytes and autoimmunity, or the induction of clonal anergy. The molecular mechanisms that maintain immunotolerance in vivo and integrate co-stimulatory signals with antigen receptor signals in T and B lymphocytes are poorly understood. Members of the Cbl/Sli family of molecular adaptors function downstream from growth factor and antigen receptors. Here we show that gene-targeted mice lacking the adaptor Cbl-b develop spontaneous autoimmunity characterized by auto-antibody production, infiltration of activated T and B lymphocytes into multiple organs, and parenchymal damage. Resting cbl-b(-/-) lymphocytes hyperproliferate upon antigen receptor stimulation, and cbl-b(-/-) T cells display specific hyperproduction of the T-cell growth factor interleukin-2, but not interferon-gamma or tumour necrosis factor-alpha. Mutation of Cbl-b uncouples T-cell proliferation, interleukin-2 production and phosphorylation of the GDP/GTP exchange factor Vav1 from the requirement for CD28 co-stimulation. Cbl-b is thus a key regulator of activation thresholds in mature lymphocytes and immunological tolerance and autoimmunity. 相似文献
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