title: 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.
abstract: 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.
authors.affiliation: Department of General Medicine, Kyushu University Hospital, Fukuoka, Japan.
authors.forename: Yong
authors.initials: Y
authors.lastname: Chong
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Ikematsu
authors.forename: Kouzaburo
authors.initials: K
authors.lastname: Yamaji
authors.forename: Mika
authors.initials: M
authors.lastname: Nishimura
authors.forename: Shigeki
authors.initials: S
authors.lastname: Nabeshima
authors.forename: Seizaburo
authors.initials: S
authors.lastname: Kashiwagi
authors.forename: Jun
authors.initials: J
authors.lastname: Hayashi
mesh_terms: D036541:ADP-ribosyl Cyclase / Q000276:immunology; D051997:ADP-ribosyl Cyclase 1; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000276:immunology*; D015703:Antigens, CD / Q000276:immunology; D017209:Apoptosis / Q000276:immunology*; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D002454:Cell Differentiation / Q000276:immunology*; D005260:Female; D006801:Humans; D007156:Immunologic Memory / Q000276:immunology; D008297:Male; D008562:Membrane Glycoproteins; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis / Q000235:genetics; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7 / Q000276:immunology*; D019014:fas Receptor / Q000276:immunology
chemical_list: D015703:Antigens, CD; D008562:Membrane Glycoproteins; D019253:Proto-Oncogene Proteins c-bcl-2; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7; D019014:fas Receptor; D036541:ADP-ribosyl Cyclase; C498154:CD38 protein, human; D051997:ADP-ribosyl Cyclase 1