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Blood, 1 March 2002, Vol. 99, No. 5, pp. 1825-1832
TRANSPLANTATION
Flt3 ligand therapy for recipients of allogeneic bone marrow
transplants expands host CD8 + dendritic cells and
reduces experimental acute graft-versus-host disease
Takanori Teshima,
Pavan Reddy,
Kathleen P. Lowler,
Mark A. KuKuruga,
Chen Liu,
Kenneth R. Cooke, and
James L. M. Ferrara
From the Departments of Internal Medicine and
Pediatrics, University of Michigan Cancer Center, Ann Arbor; and the
Department of Pathology, Immunology, and Laboratory Medicine,
University of Florida, Gainesville.
Recent evidence suggests that dendritic cells (DCs) can regulate
and amplify immune responses. Flt3 ligand (FL)-derived DC function was
tested as a stimulator of allogeneic lymphocytes in vitro and in vivo.
Treatment of mice with FL dramatically expanded DC number, but DCs
isolated from FL-treated mice (FL DCs) were poor stimulators of
allogeneic T-cell responses in vitro. Further activation of FL DCs did
not restore their stimulatory ability, and FL DCs did not suppress the
stimulation of the allogeneic T cells by normal DCs. FL treatment
significantly increased the CD8 + DC subset, which
appeared to be the reason for their poor stimulatory capacity. These
observations were confirmed in vivo using a mouse model of acute
graft-versus-host disease (GVHD) wherein host DCs play a critical role.
FL treatment of recipients before allogeneic bone marrow
transplantation dramatically suppressed donor T-cell responses to host
antigens, thereby reducing GVHD mortality (P < .01).
These data represent a novel strategy that alters host DCs and reduces
acute GVHD.
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