Department of Microbiology, Immunology and Molecular Genetics and the UCLA AIDS Institute, David Geffen School of Medicine, University of California Los Angeles, CA 90095, USA.
Proc Natl Acad Sci U S A. 2010 Feb 16;107(7):3018-23. doi: 10.1073/pnas.0914500107. Epub 2010 Jan 26.
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.
在病毒感染和接种疫苗后,引发持久免疫的关键在于产生有效的 T 细胞反应。感染后会诱导大量的抑制性和刺激性因子,正是这些信号的综合作用,对随后的效应器和记忆 T 细胞反应进行了定量和定性的编程。在淋巴细胞性脉络丛脑膜炎病毒(LCMV)感染中,免疫抑制细胞因子 IL-10 迅速上调;然而,IL-10 如何调节通常被认为是“最佳”免疫反应的机制尚不清楚。我们证明,IL-10 直接抑制急性病毒感染后的效应器和记忆 CD4 T 细胞反应。阻断 IL-10 增强了效应 CD4 T 细胞的数量和功能能力,进而导致记忆反应的增强和更有效。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,可在接种疫苗后特异性增强 CD4 T 细胞免疫和保护作用。