Institute for Biomedical Aging Research, University Innsbruck, Innsbruck, Austria.
Institute for Biomedical Aging Research, University Innsbruck, Innsbruck, Austria,
Gerontology. 2020;66(2):105-113. doi: 10.1159/000501963. Epub 2019 Sep 25.
Aging results for the immune system in a departure from the optimal homeostatic state seen in young organisms. This divergence regrettably contributes to a higher frequency of compromised responses to infections and inefficient classical vaccination in aged populations. In B cells, the cornerstone of humoral immunity, the development and distribution of the various mature B cell subsets are impacted by aging in both humans and mice. In addition, aged mature B cells demonstrate limited capacity to mount efficient antibody responses. An expected culprit for the decline in effective immunity is the rise of the systemic levels of pro-inflammatory molecules during aging, establishing a chronic low-grade inflammation. Indeed, numerous alterations affecting directly or indirectly B cells in old people and mice are reminiscent of various effects of acute inflammation on this cell type in young adults. The present mini-review will highlight the possible adverse contributions of the persistent low-level inflammation observed in susceptible older organisms to the inadequate B-cell physiology.
衰老导致免疫系统偏离年轻生物体中所见的最佳体内平衡状态。这种偏离可悲地导致感染时的反应受损频率增加,以及老年人群中经典疫苗接种效率降低。在 B 细胞中,即体液免疫的基石,各种成熟 B 细胞亚群的发育和分布都受到人类和小鼠衰老的影响。此外,衰老的成熟 B 细胞表现出产生有效抗体反应的能力有限。导致有效免疫下降的预期罪魁祸首是衰老过程中促炎分子的全身性水平升高,从而导致慢性低度炎症。事实上,许多直接或间接地影响老年人和小鼠 B 细胞的改变,类似于急性炎症对年轻人中这种细胞类型的各种影响。本综述将强调在易受影响的老年生物体中观察到的持续低度炎症对 B 细胞生理功能的不利影响。