Type I interferons act directly on CD8 T cells to allow clonal expansion and memory formation in response to viral infection.
Type I interferons act directly on CD8 T cells to allow clonal expansion and memory formation in response to viral infection.
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DOI：
10.1084/jem.20050821
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发表时间：
2005-09-05
期刊：
影响因子：
--
通讯作者：
Murali-Krishna K
中科院分区：
文献类型：
--
作者：
Kolumam GA;Thomas S;Thompson LJ;Sprent J;Murali-Krishna K
T细胞扩增和记忆形成通常在由活生物体引起时比由灭活疫苗引起时更有效。阐明潜在的机制对于疫苗接种和治疗策略是重要的。我们表明，大量的抗原特异性CD8 T细胞的扩增，发生在病毒感染的反应是严重依赖于I型干扰素（IFN-1）对CD8 T细胞的直接作用。通过使用IFN-I受体缺陷（IFN-IR 0）和足够的CD8 T细胞过继转移到正常IFN-IR野生型宿主中来检查对淋巴细胞性脉络丛脑膜炎病毒感染的反应，我们表明缺乏与IFN-I直接接触的CD8 T细胞导致其扩增和产生记忆细胞的能力降低> 99%。IFN-IR0 CD8 T细胞的扩增减少不是由增殖缺陷引起的，而是由抗原驱动的增殖阶段期间的存活率差引起的。因此，CD8 T细胞中的IFN-IR信号传导对于响应病毒感染的效应细胞和记忆细胞的产生是至关重要的。
T cell expansion and memory formation are generally more effective when elicited by live organisms than by inactivated vaccines. Elucidation of the underlying mechanisms is important for vaccination and therapeutic strategies. We show that the massive expansion of antigen-specific CD8 T cells that occurs in response to viral infection is critically dependent on the direct action of type I interferons (IFN-Is) on CD8 T cells. By examining the response to infection with lymphocytic choriomeningitis virus using IFN-I receptor–deficient (IFN-IR0) and –sufficient CD8 T cells adoptively transferred into normal IFN-IR wild-type hosts, we show that the lack of direct CD8 T cell contact with IFN-I causes >99% reduction in their capacity to expand and generate memory cells. The diminished expansion of IFN-IR0 CD8 T cells was not caused by a defect in proliferation but by poor survival during the antigen-driven proliferation phase. Thus, IFN-IR signaling in CD8 T cells is critical for the generation of effector and memory cells in response to viral infection.
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