Department of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212;
J Immunol. 2013 Dec 15;191(12):5797-801. doi: 10.4049/jimmunol.1300905. Epub 2013 Nov 15.
CD8 T cell memory critically contributes to long-term immunity. Both low- and high-affinity TCR signals are able to support the differentiation of memory CD8 T cells. However, it is unclear whether the requirements for memory development change when TCR signal strength is altered. To gain further insight into this question, we used a TCRβ transmembrane domain mutant model that is defective in the generation of memory in response to high-affinity ligands. Surprisingly, lowering TCR signal strength, by stimulation with low-affinity ligands, resulted in normal memory development. Restoration of memory correlated with recovery of TCR-dependent NF-κB signaling. Thus, these data provide novel evidence that the requirements for memory are qualitatively different depending on TCR signal strength.
CD8 T 细胞记忆对于长期免疫至关重要。低亲和性和高亲和性 TCR 信号都能够支持记忆性 CD8 T 细胞的分化。然而，当 TCR 信号强度改变时，记忆发育的要求是否会发生变化尚不清楚。为了更深入地了解这个问题，我们使用了一种 TCRβ跨膜结构域突变模型，该模型在对高亲和力配体的反应中不能产生记忆。令人惊讶的是，通过低亲和力配体的刺激降低 TCR 信号强度，导致正常的记忆发育。记忆的恢复与 TCR 依赖性 NF-κB 信号的恢复相关。因此，这些数据提供了新的证据，表明记忆的要求取决于 TCR 信号强度的定性差异。
