Transcriptional regulator Id2 mediates CD8+ T cell immunity
Transcriptional regulator Id2 mediates CD8+ T cell immunity
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DOI：
10.1038/ni1403
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发表时间：
2006-12-01
影响因子：
30.5
通讯作者：
Goldrath, Ananda W.
中科院分区：
文献类型：
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作者：
Cannarile, Michael A.;Lind, Nicholas A.;Goldrath, Ananda W.
在免疫应答期间启动和维持CD8（+）T细胞增殖、分化和存活的转录程序尚未完全理解。在此，我们发现DNA结合抑制剂2（Id2），一种E蛋白转录因子的拮抗剂，在感染过程中在CD8（+）T细胞中上调，并且Id2的表达在记忆性CD8（+）T细胞中得以维持。虽然Id2缺陷型初始CD8（+）T细胞在感染后早期识别抗原并正常增殖，但效应CD8+ T细胞不积累，因为细胞对凋亡高度敏感。Id2缺陷型CD8（+）T细胞对感染的反应改变了影响生存的基因表达，并改变了记忆形成。我们的数据强调ld2在调节基因表达的CD8+ T细胞和效应反应的幅度的重要性，表明机制涉及Id蛋白和E蛋白介导的生存和分化的成熟T细胞。
Transcriptional programs that initiate and sustain the proliferation, differentiation and survival of CD8(+) T cells during immune responses are not completely understood. Here we show that inhibitor of DNA binding 2 (Id2), an antagonist of E protein transcription factors, was upregulated in CD8(+) T cells during infection and that expression of Id2 was maintained in memory CD8(+) T cells. Although Id2-deficient naive CD8(+) T cells recognized antigen and proliferated normally early after infection, effector CD8+ T cells did not accumulate because the cells were highly susceptible to apoptosis. Id2-deficient CD8(+) T cells responding to infection had changes in the expression of genes that influence survival and had altered memory formation. Our data emphasize the importance of ld2 in regulating gene expression by CD8+ T cells and the magnitude of effector responses, suggesting a mechanism involving Id protein- and E protein-mediated survival and differentiation of mature T cells.