Different repopulation kinetics of erythroid (BFU‐E), myeloid (CFU‐GM) and T lymphocyte (TL‐CFU) progenitor cells after autologous and allogeneic bone marrow transplantation

Marrow recovery of erythroid (BFU‐E). myeloid (CFIJ‐GM) and T‐lymphocyte (TL‐CFU) progenitor cells was studied at various time intervals after autologous bone marrow transplantation in 10 patients with acute myeloid leukaemia in remission. These data were compared with those in 14 recipients of T‐cell depleted allogeneic marrow grafts. The results indicate markedly different repopulation kinetics of BFIJ‐E. CFU‐GM and TL‐CFU after autologous and allogeneic bone marrow transplantation. Following auto‐grafting reduced numbers of BFU‐E and CFU‐GM were always present at 2 months after transplantation. Between 2–6 and 6–24 months a gradual increase occurred, although reduced BFU‐E and CFU‐GM values were stil noted in 50% of the cases in spite of normal bone marrow cellularity and restoration of peripheral blood counts. In contrast. in the allograft recipients normal BFU‐E numbers appeared within 2 months after transplantation. In addition, CFU‐GM values had become normal in 3 5% of the tests performed at 1 ‐2 months and respectively in 66% and 100% at 2–6 and 6–24 months. The recovery pattern of TL‐CFU differed from that of the other haemopoietic progenitor cells. TL‐CFU showed a fast recovery, i.e. within 1 month after autologous bone marrow transplantation which was much more rapid than that of BFU‐E and CFU‐GM. After allografting. however, TL‐CFU regenerated at a slower rate and reached normal levels between 2 and 6 months after transplantation. We suggest that the delayed restoration of myeloid and erythroid progenitor cells after autologous transplantation is related to a proliferative defect of the graft as a result of the preceding cytotoxic chemotherapy, the underlying malignant disease and/or cyropreservation. The slower recovery of the T lymphocyte precursors after allografting might be due to the immunological interactions between graft and host, the immuno‐suppressive therapy and/or the in vitro T cell depletion of the graft. Copyright

• View at Publisher
• View at Pubmed
• View at Scopus