Helena Slaets, Naomi Veeningen, Peter L. J. de Keizer, Niels Hellings, Sven Hendrix
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引用次数: 0
摘要
正常 T 细胞功能的丧失是衰老的一个特征,会增加罹患慢性疾病的风险。在老年人体内,高度分化的 T 细胞会出现 CD28 和 CD27 表达减少、KLRG-1 或 CD57 表达增加的现象。这些细胞通常被称为免疫衰老 T 细胞,但仍可能具有高度活性并导致自身免疫。另一种被称为衰竭 T 细胞的 T 细胞群在长期抗原刺激后出现,并失去效应功能,导致无法对抗恶性肿瘤和病毒感染。在衰老过程中,一种被称为细胞衰老的过程也会加剧,针对这一过程进行治疗已被证明在动物模型中对一系列与衰老相关的病症有很好的疗效。细胞衰老发生在受到不可修复损伤的细胞中,限制了它们的增殖,通常会导致促炎因子的长期分泌。要开发针对 T 细胞功能缺陷引起的病症的疗法,了解免疫衰老和细胞衰老之间的异同非常重要。在此,我们回顾了细胞衰老与衰老和衰竭 T 细胞的特征,并为开发针对老年相关疾病的特定疗法提供了参考。
Loss of proper T-cell functioning is a feature of aging that increases the risk of developing chronic diseases. In aged individuals, highly differentiated T cells arise with a reduced expression of CD28 and CD27 and an increased expression of KLRG-1 or CD57. These cells are often referred to as immunosenescent T cells but may still be highly active and contribute to autoimmunity. Another population of T cells known as exhausted T cells arises after chronic antigen stimulation and loses its effector functions, leading to a failure to combat malignancies and viral infections. A process called cellular senescence also increases during aging, and targeting this process has proven to be fruitful against a range of age-related pathologies in animal models. Cellular senescence occurs in cells that are irreparably damaged, limiting their proliferation and typically leading to chronic secretion of pro-inflammatory factors. To develop therapies against pathologies caused by defective T-cell function, it is important to understand the differences and similarities between immunosenescence and cellular senescence. Here, we review the hallmarks of cellular senescence versus senescent and exhausted T cells and provide considerations for the development of specific therapies against age-related diseases.
期刊介绍:
Aging Cell, an Open Access journal, delves into fundamental aspects of aging biology. It comprehensively explores geroscience, emphasizing research on the mechanisms underlying the aging process and the connections between aging and age-related diseases.