Intra‐bone marrow bone marrow transplantation rejuvenates the B‐cell lineage in aged mice
Age‐related reductions in the frequency and absolute number of early B lineage precursors in the bone marrow of aged mice have been reported. Reversal of B‐cell lineage senescence has not been achieved. Age‐related impairment of the B‐cell lineage is caused by the decreasing functionality of hematop...
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Veröffentlicht in: | Immunology and cell biology 2010-01, Vol.88 (1), p.87-94 |
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Zusammenfassung: | Age‐related reductions in the frequency and absolute number of early B lineage precursors in the bone marrow of aged mice have been reported. Reversal of B‐cell lineage senescence has not been achieved. Age‐related impairment of the B‐cell lineage is caused by the decreasing functionality of hematopoietic and B lineage precursors, and reduced efficacy of bone marrow stromal cells that constitute the bone marrow microenvironment. To induce rejuvenation of aged B cells, we injected whole bone marrow from young donors to irradiated aged recipients through the tibia and analyzed B‐cell development and immune responsiveness. In aged mice, we found significant reductions in the frequencies and absolute numbers of pro‐B cells (B220+CD43+CD24+BP‐1− and B220+CD43+CD24intBP‐1+) and pre‐B cells (B220+CD43+CD24highBP‐1+ and B220+CD43−IgM−IgD−). Intra‐bone marrow bone marrow transplantation (IBM‐BMT) of young marrow cells including both hematopoietic stem cells and bone marrow stromal cells reversed the reduction of pro‐B cells and pre‐B cells. In the periphery, the frequency and absolute number of marginal zone‐B cell were not significantly different between young, old and IBM‐BMT group. The frequency of follicular‐B cells in the IBM‐BMT group was significantly increased compared to old group. The frequency of B1a B cells in the peritoneal cavity was significantly decreased in the IBM‐BMT group. Antibody production against T‐independent antigens was not different among the young, the aged and IBM‐BMT groups. |
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ISSN: | 0818-9641 1440-1711 |
DOI: | 10.1038/icb.2009.69 |