Division of Infectious Diseases, 3333 Burnet Ave., MLC 7017, Cincinnati, OH 45229, USA.
J Leukoc Biol. 2013 Aug;94(2):367-76. doi: 10.1189/jlb.0313118. Epub 2013 Jun 6.
Although T cell activation has been classically described to require distinct, positive stimulation signals that include B7-1 (CD80) and B7-2 (CD86) costimulation, overriding suppression signals that avert immune-mediated host injury are equally important. How these opposing stimulation and suppression signals work together remains incompletely defined. Our recent studies demonstrate that CD8 Teff activation in response to cognate peptide stimulation is actively suppressed by the Foxp3(+) subset of CD4 cells, called Tregs. Here, we show that the elimination of Treg suppression does not bypass the requirement for positive B7-1/B7-2 costimulation. The expansion, IFN-γ cytokine production, cytolytic, and protective features of antigen-specific CD8 T cells stimulated with purified cognate peptide in Treg-ablated mice were each neutralized effectively by CTLA-4-Ig that blocks B7-1/B7-2. In turn, given the efficiency whereby CTLA-4-Ig overrides the effects of Treg ablation, the role of Foxp3(+) cell-intrinsic CTLA-4 in mitigating CD8 Teff activation was also investigated. With the use of mixed chimera mice that contain CTLA-4-deficient Tregs exclusively after the ablation of WT Foxp3(+) cells, a critical role for Treg CTLA-4 in suppressing the expansion, cytokine production, cytotoxicity, and protective features of peptide-stimulated CD8 T cells is revealed. Thus, the activation of protective CD8 T cells requires positive B7-1/B7-2 costimulation even when suppression by Tregs and in particular, Treg-intrinsic CTLA-4 is circumvented.
虽然 T 细胞的激活已被经典地描述为需要独特的正刺激信号,包括 B7-1(CD80)和 B7-2(CD86)共刺激,但规避避免免疫介导的宿主损伤的抑制信号同样重要。这些相反的刺激和抑制信号如何协同工作仍不完全清楚。我们最近的研究表明,CD8 Teff 对同源肽刺激的激活被称为 Treg 的 Foxp3(+)亚群的 CD4 细胞主动抑制。在这里,我们表明消除 Treg 抑制并没有绕过对正 B7-1/B7-2 共刺激的要求。在 Treg 耗竭小鼠中用纯化的同源肽刺激的抗原特异性 CD8 T 细胞的扩增、IFN-γ细胞因子产生、细胞毒性和保护特征,都被阻断 B7-1/B7-2 的 CTLA-4-Ig 有效中和。反过来,鉴于 CTLA-4-Ig 克服 Treg 耗竭影响的效率,还研究了 Foxp3(+)细胞内源性 CTLA-4 在减轻 CD8 Teff 激活中的作用。使用混合嵌合体小鼠,在 WT Foxp3(+)细胞耗竭后仅含有 CTLA-4 缺陷的 Treg,揭示了 Treg CTLA-4 在抑制肽刺激的 CD8 T 细胞扩增、细胞因子产生、细胞毒性和保护特征中的关键作用。因此,即使规避了 Treg 的抑制作用,尤其是 Treg 内源性 CTLA-4 的抑制作用,保护性 CD8 T 细胞的激活也需要正 B7-1/B7-2 共刺激。