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衰老的BALB/c小鼠中B细胞前体减少,但在体内和体外均保持正常的有丝分裂活性。

B cell precursors are decreased in senescent BALB/c mice, but retain normal mitotic activity in vivo and in vitro.

作者信息

Riley R L, Kruger M G, Elia J

机构信息

Department of Microbiology and Immunology, University of Miami School of Medicine, Florida 33101.

出版信息

Clin Immunol Immunopathol. 1991 May;59(2):301-13. doi: 10.1016/0090-1229(91)90026-7.

Abstract

The numbers of phenotypic (sIg- Ly5[220]+) and functional B cell precursors were significantly reduced in the bone marrow of senescent (22-24 months old) BALB/c mice when compared to their young (2-4 months old) cohorts. Little alteration in the numbers of B cell precursors occurred during the first 12 months of life in this strain. In contrast, an accelerated loss of B cell precursors between 15 and 18 months of age was observed. In particular, the levels of small Ly5(220)+ B cell precursors were decreased with advanced age, although a decline in numbers of large sIg- Ly5(220)+ B cell precursors was also evident. The percentages of large sIg- Ly5(220)+ B cell precursors in (S + G2/M) stages of cell cycle were similar (e.g., 60-80%) in aged and young BALB/c mice. Importantly, Ly5(220)+ pre-B cells from both young and aged BALB/c mice, either present in vivo or derived from Ly5(220)- cells in vitro, were capable of proliferation in response to rIL-7. These observations suggest that the aging process results in a progressive decline in the numbers of pre-B cells; however, this apparently is not due to failure of B lineage precursor cells to respond to growth mediators either in vivo or in vitro.

摘要

与年轻(2 - 4个月大)的BALB/c小鼠相比,衰老(22 - 24个月大)的BALB/c小鼠骨髓中表型(sIg - Ly5[220]+)和功能性B细胞前体的数量显著减少。在该品系小鼠生命的前12个月中,B细胞前体数量几乎没有变化。相反,在15至18个月龄之间观察到B细胞前体加速减少。特别是,随着年龄增长,小Ly5(220)+ B细胞前体水平下降,尽管大sIg - Ly5(220)+ B细胞前体数量的减少也很明显。在衰老和年轻的BALB/c小鼠中,处于细胞周期(S + G2/M)阶段的大sIg - Ly5(220)+ B细胞前体的百分比相似(例如,60 - 80%)。重要的是,来自年轻和衰老BALB/c小鼠的Ly5(220)+ 前B细胞,无论是体内存在的还是体外从Ly5(220)- 细胞衍生而来的,都能够对rIL - 7作出增殖反应。这些观察结果表明,衰老过程导致前B细胞数量逐渐减少;然而,这显然不是由于B系前体细胞在体内或体外对生长介质无反应所致。

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