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F(ab')2 Prevents Graft-Versus-Host Disease by Selectively Depleting Donor T Cells Activated by Recipient Alloantigens1
*
Fred Hutchinson Cancer Research Center, Seattle, WA 98109; and
Department of Medicine, University of Washington, Seattle, WA 98195
Transplantation tolerance is facilitated by activation-induced
apoptosis of peripheral T cells triggered by specific Ag. Abs specific
for the nonpolymorphic CD3 component of the TCR complex bind to APCs
through Fc-FcR interactions, mimic MHC-peptide, and activate polyclonal
T cells. In contrast, F(ab')2 of anti-CD3
Abs do not
activate naive T cells but induce apoptosis of Ag-activated, cycling T
cells. Here, we report that treatment with anti-CD3
F(ab')2 can selectively induce apoptosis of donor T cells
that recognize a recipient alloantigen, thereby preventing
graft-vs-host disease initiated by a TCR-transgenic T cell population.
The selective elimination of Ag-activated T cells by non-FcR-binding
anti-CD3
Abs could serve as an ideal strategy to prevent
graft-vs-host disease and allograft rejection or to treat autoimmune
disorders.
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