Immunoaging induced by hematopoietic stem cell aging

被引：79

作者：

Wang, Jianwei ^{[1
]}

Geiger, Hartmut ^{[2
,3
]}

Rudolph, K. Lenhard ^{[1
]}

机构：

[1] Univ Ulm, Inst Mol Med & Max Planck Res, Dept Stem Cell Aging, Ulm, Germany

[2] Univ Ulm, Dept Dermatol & Allerg Dis, Ulm, Germany

[3] Cincinnati Childrens Hosp Med Ctr, Div Expt Hematol & Canc Biol, Cincinnati, OH USA

来源：

CURRENT OPINION IN IMMUNOLOGY | 2011年 / 23卷 / 04期

关键词：

DNA-DAMAGE; LIFE-SPAN; TELOMERE DYSFUNCTION; LYMPHOID PROGENITORS; SELF-RENEWAL; AGED MICE; COMPARTMENT; CANCER; REPAIR; LEUKEMOGENESIS;

D O I：

10.1016/j.coi.2011.05.004

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Hematopoietic stem cells (HSCs) generate all known hematopoietic lineages and self-renew, but the function of HSCs declines during aging, which is characterized as impairments of lymphopoiesis and enhanced myelopoiesis. These aging-associated changes correlate with an increasing risk of myelo-proliferative diseases and impairments in immune function. Recent studies showed that only a subpopulation of HSCs contains a high capacity to undergo lymphoid differentiation but this subpopulation is lost during aging, which contributes to age-related impairments in lymphopoiesis. On the basis of the observations that DNA damage and telomere dysfunction can impair stem cell function, it is possible that accumulation of DNA damage results in the loss of subpopulations of HSCs that are required for the maintenance of lymphopoiesis and immune functions during aging.

引用

页码：532 / 536

页数：5

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