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中华危重症医学杂志(电子版) ›› 2021, Vol. 14 ›› Issue (01) : 3 -9. doi: 10.3877/cma.j.issn.1674-6880.2021.01.001

所属专题: 文献

免疫衰老与脓毒症

增龄性免疫衰老与免疫抑制网络
徐佳1, 陆远强1,()   
  1. 1. 310003 杭州,浙江大学医学院附属第一医院急诊科、浙江省增龄与理化损伤性疾病诊治研究重点实验室
  • 收稿日期:2021-01-05 出版日期:2021-02-28
  • 通信作者: 陆远强
  • 基金资助:
    国家自然科学基金项目(81801572、81272075); "十三五"浙江省中医药(中西医结合)重点学科项目(2017-XKA36)

Age-related immunosenescence and immunosuppressive network

Jia Xu1, Yuanqiang Lu1,()   

  1. 1. Department of Emergency Medicine, Zhejiang Provincial Key Laboratory for Diagnosis and Treatment of Aging and Physic-chemical Injury Diseases, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China
  • Received:2021-01-05 Published:2021-02-28
  • Corresponding author: Yuanqiang Lu
引用本文:

徐佳, 陆远强. 增龄性免疫衰老与免疫抑制网络[J]. 中华危重症医学杂志(电子版), 2021, 14(01): 3-9.

Jia Xu, Yuanqiang Lu. Age-related immunosenescence and immunosuppressive network[J]. Chinese Journal of Critical Care Medicine(Electronic Edition), 2021, 14(01): 3-9.

随着社会老龄化的加重,增龄性免疫衰老研究已经成为国际上新的热点。免疫衰老是导致老年人感染、肿瘤和自身免疫性疾病发病率和病死率居高不下的重要因素,与疫苗接种效率下降及2型糖尿病、动脉粥样硬化、骨质疏松、关节炎等衰老相关疾病密切相关。目前,转录调控、染色质重塑、自噬、泛素-蛋白酶体系统、氧化应激等领域已对免疫衰老机制有所阐释。但免疫衰老并非整体免疫功能不可逆的损伤和下降,而是机体免疫系统经过长期适应性精密调整和重塑的结果。早在二十世纪七十年代,研究者们已发现免疫衰老可能是由免疫抑制细胞活性的提高,而不是由免疫细胞的衰老所引起的。因此,本文将从增龄性免疫微环境的改变和免疫抑制网络活化的角度对免疫衰老的可能机制进行综述。

With the aggravation of the aging society, the research of age-related immunesenescence has become a new research focus worldwide. Immunesenescence is an important factor leading to the high incidence and mortality of infections, tumors and autoimmune diseases in the elderly. It is closely related to the decline in vaccination efficiency and aging-related diseases such as type 2 diabetes, atherosclerosis, osteoporosis and arthritis. At present, the mechanism of immunesenescence has been explained in the fields of transcriptional regulation, chromatin remodeling, autophagy, ubiquitin-proteasomal system, oxidative stress, and so on. However, immunesenescence is not the irreversible damage and decline of overall immune functions, but the result of long-term adaptive fine adjustment and remodeling of immune system. Evidence has accumulated since the 1970's indicating that immunosenescence might be caused by an increased activity of immunosuppressive cells rather than cellular senescence. Therefore, this article reviews the possible mechanisms of immune aging from the perspectives of the aging-related immune microenvironment changes and activation of immune suppression network.

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