CD27(+) (memory) B cell decrease and apoptosis-resistant CD27(-) (naive) B cell increase in aged humans: implications for age-related peripheral B cell developmental disturbances.

نویسندگان

  • Yong Chong
  • Hideyuki Ikematsu
  • Kouzaburo Yamaji
  • Mika Nishimura
  • Shigeki Nabeshima
  • Seizaburo Kashiwagi
  • Jun Hayashi
چکیده

To investigate age-related alterations in human humoral immunity, we analyzed the quantity and quality of peripheral B cell subsets, CD27-negative (CD27(-)) and CD27-positive (CD27(+)) B cells, by flow cytometry analysis in 54 aged individuals (mean age +/- SE, 74.6 +/- 0.7 years) and 30 young individuals (mean age +/- SE, 26.1 +/- 0.5 years). CD27(-) and CD27(+) B cells are regarded as naive and memory B cells, respectively. CD38, Ki-67, CD95 and bcl-2 were used as activation, proliferation and apoptotic markers. Susceptibility to apoptosis was evaluated by cell size and annexin-V binding in culture cells. The percentage of CD27(+) B cells was significantly lower in aged (mean, 19.2%) individuals than that in young individuals (mean, 28.2%). The opposite was true for CD27(-) B cells (mean, 80.8% in aged and 71.8% in young) (P < 0.01). The absolute number of CD27(+) B cells in aged individuals was significantly less than the number of CD27(-) B cells. The CD27(+) B cells from aged individuals showed little susceptibility to apoptosis, although CD95 expression on the CD27(+) B cells was significantly higher in the aged individuals than in the young individuals (P < 0.05). The CD38 and bcl-2 expression on the CD27(-) B cells was significantly higher in the aged individuals than in the young individuals (P < 0.05). In addition, the CD27(-) B cells from the aged individuals showed a decreased susceptibility to apoptosis compared with that of the young individuals. These findings suggested that human aging leads to both quantitative and qualitative alterations in the peripheral B cell developmental system, including memory and naive B cell balance and their surface phenotypes.

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عنوان ژورنال:
  • International immunology

دوره 17 4  شماره 

صفحات  -

تاریخ انتشار 2005