CD8 Tau cell contraction and memory formation

免疫系统的适应性分支由B和T淋巴细胞组成。CD8 T细胞是关键 参与调节对细胞内病原体和肿瘤的免疫。CDS T细胞在体内遇到抗原 MHC I类的上下文被激活，并启动一个增殖和分化为 效应细胞毒性T淋巴细胞(CTL)。通常，为了应对急性病毒感染，幼稚的CDS T细胞 可能在6天内经过15个以上的分裂，产生数千个效应器后代。在…的巅峰时期 这种反应，也被称为主要反应，通常在接下来的几天内清除抗原 超过90%的效应器CDS T细胞死亡。这个被称为收缩的过程留下了一个幸存的 作为长寿记忆细胞存留的T细胞的一部分。除了它们的寿命之外，记忆单元还有 进一步的特点是它们能够以增强的效力响应相同的抗原重新攻击 (二次回应)。这些功能，加上它们数量的增加，允许记忆CD8+T细胞提供 针对以前遇到的病原体的高效持久免疫。 虽然许多已建立的疫苗接种计划主要依赖于有效的抗体反应， 疟疾、艾滋病毒和结核病等联合国挑战似乎需要一种不同的方法。CDS T 细胞是保护我们免受细胞内病原体(如病毒或某些细胞内病原体)侵袭的关键角色 细菌)。彻底了解CDS T细胞记忆是如何产生和维持的将为我们提供 有更多的洞察力和更好的疫苗接种策略。 我们希望将我们的研究重点放在CDS T细胞反应中知之甚少的收缩部分。 我研究的主要目标是了解CDS T细胞如何从效应者转变为 调整存储阶段以及如何生成合适的存储T细胞池。更具体的目标是 未来两年将阐明控制收缩阶段某些方面的机制和 CDS T细胞反应的后续记忆阶段。

The adaptive branch of the immune system consists of B and T lymphocytes. CD8 T cells are key players in mediating immunity to Intracellular pathogens and tumors. CDS T cells that encounter antigen in the context of MHC class I become activated and initiate a program of proliferation and differentiation into effector cytotoxic T lymphocytes (CTL). Typically, in response to an acute viral infection, a naive CDS T cell may go through more than 15 divisions in 6 days to generate thousands of effector progeny. At the peak of this response, also called the primary response, antigen has typically been cleared and in the following days more than 90% of the effector CDS T cells die. This process called contraction leaves behind a surviving fraction of T cells that persists as long-lived memory cells. Apart from their longevity, memory cells are further characterized by their ability to respond with enhanced efficacy to rechallenge with the same antigen (secondary response). These features, plus their increased numbers, allow memory CD8+ T cell to provide efficient long lasting immunity against previously encountered pathogens. While many established vaccination programs are mainly dependent on an efficient antibody response, cun^ent challenges such as malaria, HIV and tuberculosis appear to require a different approach. CDS T cells are a key player protecting us against intracellular pathogens (such as viruses or certain intracellular bacteria). A thorough understanding of how CDS T cell memory is generated and maintained will provide us with more insight and better vaccination strategies. We want to focus our research on the poorly understood contraction part of the CDS T cell response. The broad goal of my research is to understand how the transition of CDS T cells from the effector to the memory stage is regulated and how a fit memory T cell pool is generated. The more specific goal for the next two years is to shed light on the mechanisms that control certain aspects of the contraction phase and the ensuing memory phase of the CDS T cell response.