In vitro evidence for disappearance of erythroid progenitor T suppressor
cells following allogeneic bone marrow transplantation for severe aplastic
anemia
KF Mangan, MT Mullaney, CS Rosenfeld and RK Shadduck
Pittsburgh Cancer Institute Bone Marrow Transplant Program, Montefiore
Hospital, University of Pittsburgh School of Medicine, PA.
In vitro coculture studies were performed in five patients with severe
aplastic anemia (SAA) and their normal HLA-matched donors before and after
allogeneic bone marrow transplantation (BMT) to determine whether the
erythropoietic function of T cells is abnormal in this disorder. These
coculture studies used fresh or cryopreserved marrow T lymphocytes with
fresh or cryopreserved marrow T cell-depleted target cells. Four of five
aplastic patients had little or no transfusion exposure before studies. The
composite results showed that, in comparison to the erythropoietic effects
of normal HLA-identical marrow T lymphocytes or engrafted T lymphocytes, T
lymphocytes collected from the aplastic patients before BMT consistently
suppressed or failed to support CFUE and BFUE growth optimally from
autologous marrow, HLA- identical marrow, or engrafted aplastic T
cell-depleted marrows. This T cell abnormality was not observed in four
multiply transfused leukemics and three patients with myelodysplastic
syndrome. Marker analyses of SAA marrow T lymphocytes performed before and
after BMT suggested that the erythropoietic functional abnormality was due
to abnormal marrow T cell composition reflecting an excess of activated
Tac+, T3+, T11+ lymphocytes. Collectively, these in vitro studies provide
firmer in vitro evidence implicating T cells in the pathogenesis of SAA.
The erythropoietic T cells abnormalities in SAA are fully corrected by
allogeneic BMT.
Volume 71,
Issue 1,
pp. 144-150,
01/01/1988
Copyright © 1988 by The American Society of Hematology
