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Prepublished online as a Blood First Edition Paper on October 17, 2002; DOI 10.1182/blood-2002-05-1529.
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Blood, 1 March 2003, Vol. 101, No. 5, pp. 2033-2042
TRANSPLANTATION
Donor pretreatment with progenipoietin-1 is superior to
granulocyte colony-stimulating factor in preventing graft-versus-host
disease after allogeneic stem cell transplantation
Kelli P. A. MacDonald,
Vanessa Rowe,
Cheryl Filippich,
Ranjeny Thomas,
Andrew D. Clouston,
Joseph K. Welply,
Derek N. J. Hart,
James L. M. Ferrara, and
Geoffrey R. Hill
From The Queensland Institute of Medical Research, and
the Department of Pathology, University of Queensland, Herston,
Australia; the Mater Medical Research Institute, South
Brisbane, Australia; the Centre for Immunology and Cancer
Research, Princess Alexandra Hospital, Woolloongabba,
Australia; the Department of Oncology, Pharmacia, St
Louis, MO; the Department of Internal Medicine and Pediatrics,
University of Michigan, Ann Arbor, MI; and the Department of Stem Cell
Transplantation, Royal Brisbane Hospital, Brisbane,
Australia.
The granulocyte colony-stimulating factor (G-CSF) and
Flt-3 receptor agonist progenipoietin-1 (ProGP-1) has potent
effects on dendritic cell (DC) expansion and may be an alternative to G-CSF for the mobilization of stem cells for allogeneic stem cell transplantation (SCT). We studied the ability of stem cell grafts mobilized with this agent to induce graft-versus-host disease (GVHD) to
minor and major histocompatibility antigens in the well-described B6  B6D2F1 SCT model. ProGP-1, G-CSF, or control diluent was administered to donor B6 mice. ProGP-1 expanded all cell lineages in
the spleen, and unseparated splenocytes from these animals produced
large amounts of interleukin 10 (IL-10) and transforming growth factor
beta (TGF ) whereas the expression of T-cell adhesion molecules was
diminished. Transplantation survival was 0%, 50%, and 90% in
recipients of control-, G-CSF-, and ProGP-1-treated allogeneic donor
splenocytes, respectively (P < .0001). Donor pretreatment with ProGP-1 allowed a 4-fold escalation in T-cell dose
over that possible with G-CSF. Donor CD4 T cells from allogeneic SCT
recipients of ProGP-1 splenocytes demonstrated an anergic response to
host antigen, and cytokine production (interferon gamma [IFN ],
IL-4, and IL-10) was also reduced while CD8 T-cell cytotoxicity to host
antigens remained intact. Neither CD11chi DCs nor
CD11cdim/B220hi DCs from ProGP-1-treated
animals conferred protection from GVHD when added to control spleen.
Conversely, when equal numbers of purified T cells from control-,
G-CSF-, or ProGP-1-treated allogeneic donors were added to allogeneic
T-cell-depleted control spleen, survival at day 60 was 0%, 15%, and
90%, respectively (P < .0001). The improved survival in
recipients of ProGP-1 T cells was associated with reductions in
systemic tumor necrosis factor alpha generation and GVHD of the
gastrointestinal tract. We conclude that donor pretreatment with
ProGP-1 is superior to G-CSF for the prevention of GVHD after
allogeneic SCT, primarily due to incremental affects on T-cell
phenotype and function.
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