CTLA-4 (CD152)-induced signaling pathways as regulators of CD8+ T lymphocytes (B14)

为了防止免疫病理，CD8+ T细胞的分化受到抑制受体（如CTLA-4）的严格控制。项目B14与B16合作，通过iTRAQ质谱鉴定了CTLA-4下游的新型信号转导途径，将在第三个资助期进一步表征。在这方面，B14将细胞代谢的变化与T细胞功能的改变联系起来。ctla -4介导的TCF-1调控在记忆形成中的作用将在李斯特菌感染模型中与A05合作进行分析。此外，B14将与B08和B12合作，分析CTLA-4在共刺激和粘附的情况下对JAML的影响。

To prevent immunopathology, differentiation of CD8+ T cells is tightly controlled by inhibitory receptors such as CTLA-4. Project B14, in collaboration with B16, identified by iTRAQ mass spectrometry novel signal transduction pathways downstream of CTLA-4 that will be further characterized in the 3rd funding period. In this respect, B14 will connect changes in cellular metabolism with altered T cell functions. The role of CTLA-4-mediated TCF-1 regulation in memory formation will be analyzed in a Listeria infection model in collaboration with A05. Furthermore, B14 will analyze the impact of CTLA-4 on JAML in the context of co-stimulation and adhesion in collaboration with B08 and B12.