Introduction: With age, the proportion of memory T cells increases, while the proportion and number of naive T cell decreases. Memory T cells are more sensitive to antigenic stimulation and less dependent on co-stimulation signals, as compared to naïve T cells. Differentiation of naïve T cells into memory T cells is accompanied by an increase in T cell reactivity to self-peptide/MHC complexes, which allowed for positive selection of their naïve precursors in the thymus.Areas covered: We envisage that in geriatric age memory Th1-type autoreactivity leads to age-associated immune hyporeactivity, atherosclerosis, and degenerative neuropathology, such as Alzheimer's and Parkinson's diseases, whereas autoreactive memory Th2 cells could promote tumorigenesis.Expert option: Stimulation of adaptive immunoregulatory mechanisms by polyclonal T-cell vaccination could constrain the development of age-related T-cell autoreactivity surplus. Another approach to immune system 'rejuvenation' could involve adoptive cell transfer of naïve T cells with a view to restrain the expansion of pathological memory T cells and support immune responsiveness to novel antigenic challenges. The proposed concept conjectures the occurrence of a hard-wired immunological clock that could determine the duration of life, which theoretically could be subject to immune-based therapy.

中文翻译：

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免疫记忆限制了人类的寿命：记忆СD4+ T细胞在与年龄相关的免疫异常中的作用。

简介：随着年龄的增长，记忆T细胞的比例增加，而幼稚T细胞的比例和数量减少。与幼稚的T细胞相比，记忆T细胞对抗原刺激更敏感，对共刺激信号的依赖性更小。幼稚T细胞分化为记忆性T细胞时，伴随着T细胞对自身肽/ MHC复合物的反应性增加，从而可以在胸腺中对其幼稚前体进行阳性选择。型自身反应性导致与年龄相关的免疫反应性低下，动脉粥样硬化和变性神经病理学，例如阿尔茨海默氏病和帕金森氏病，而自身反应性记忆Th2细胞可促进肿瘤发生。多克隆T细胞疫苗接种刺激适应性免疫调节机制可能会限制与年龄相关的T细胞自身反应性过剩的发展。免疫系统“恢复活力”的另一种方法可能涉及幼稚T细胞的过继性细胞转移，以抑制病理记忆T细胞的扩增并支持对新抗原挑战的免疫应答。提出的概念推测出硬连线的免疫时钟的出现可以确定生命的持续时间，理论上该生命可以接受基于免疫的治疗。为了抑制病理性记忆T细胞的扩增并支持对新抗原挑战的免疫应答，可能涉及幼稚T细胞的过继细胞转移。提出的概念推测出可以确定寿命的硬连线免疫时钟的发生，理论上该寿命可以接受基于免疫的治疗。为了抑制病理性记忆T细胞的扩增并支持对新抗原挑战的免疫应答，可能涉及幼稚T细胞的过继细胞转移。提出的概念推测出可以确定寿命的硬连线免疫时钟的发生，理论上该寿命可以接受基于免疫的治疗。