首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >IL-10 directly suppresses CD4 but not CD8 T cell effector and memory responses following acute viral infection
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IL-10 directly suppresses CD4 but not CD8 T cell effector and memory responses following acute viral infection

机译:IL-10直接抑制CD4但不抑制CD8 T细胞效应子和急性病毒感染后的记忆反应

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摘要

Mounting effective T cell responses is critical for eliciting long-lasting immunity following viral infection and vaccination. A multitude of inhibitory and stimulatory factors are induced following infection, and it is the compilation of these signals that quantitatively and qualitatively program the ensuing effector and memory T cell response. In response to lymphocytic choriomeningitis virus (LCMV) infection, the immunosuppressive cytokine IL-10 is rapidly up-regulated; however, how IL-10 is regulating what is often considered an “optimal” immune response is unclear. We demonstrate that IL-10 directly inhibits effector and memory CD4 T cell responses following an acutely resolved viral infection. Blockade of IL-10 enhanced the magnitude and the functional capacity of effector CD4 T cells that translated into increased and more effective memory responses. On the other hand, lack of IL-10 signaling did not impact memory CD8 T cell development. We propose that blockade of IL-10 may be an effective adjuvant to specifically enhance CD4 T cell immunity and protection following vaccination.
机译:建立有效的T细胞反应对于在病毒感染和疫苗接种后引起持久的免疫力至关重要。感染后会诱导出多种抑制和刺激因子,正是这些信号的汇集对定性的随后的效应子和记忆T细胞反应进行了定量和定性编程。响应淋巴细胞性脉络膜脑膜炎病毒(LCMV)感染,免疫抑制性细胞因子IL-10迅速上调;但是,IL-10如何调节通常被认为是“最佳”的免疫反应尚不清楚。我们证明IL-10直接抑制急性解决病毒感染后的效应和记忆CD4 T细胞反应。 IL-10的阻滞增强了效应器CD4 T细胞的大小和功能能力,后者转化为更多且更有效的记忆反应。另一方面,缺乏IL-10信号传导不会影响记忆CD8 T细胞的发育。我们提出,阻断IL-10可能是一种有效的佐剂,可以在接种疫苗后特异性增强CD4 T细胞的免疫力和保护作用。

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