International Journal of Cell Cloning, Vol 5, 450-462, Copyright © 1987 by AlphaMed Press
Hematopoietic factors in graft-versus-host reaction
A Kanamaru and H Hara
Second Department of Internal Medicine, Hyogo College of Medicine, Japan.
Graft-versus-host (GVH) reaction has a curious unsolved area in the
immunopathogenesis and pathophysiology of the immunohematopoietic system,
and GVH disease remains one of the major obstacles in clinical allogeneic
bone marrow transplantation. T lymphocytes and T lymphocyte subpopulations
are now recognized to be initiators of this GVH reaction and disease. Also,
T lymphocytes are known to be accessory cells in the regulation of
hematopoiesis, and produce a variety of lymphokines relevant to
hematopoiesis. Admittedly, remarkable hematopoietic changes can be found in
GVH reaction, but the cellular mechanisms underlying these changes are so
complex they have yet to be fully elucidated. In fact, elevated serum
levels of myeloid and erythroid colony-stimulating activities were found in
mice suffering from GVH disease in which marked granulopoiesis and
suppression of erythropoietic differentiation were seen. In addition, each
granulocyte/macrophage colony-stimulating factor (GM-CSF) or
burst-promoting activity (BPA) could be detected in sera from patients with
GVH disease following allogeneic bone marrow transplantation. There seems
to be at least two mechanisms involved in the control of hematopoiesis with
either humoral or local environmental factor, probably via the T
lymphocytes or T lymphocyte subpopulations activated by alloantigens or
autologous non-T cells.
