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Blood, Vol. 94 No. 2 (July 15), 1999:
pp. 390-400
Massive Activation-Induced Cell Death of Alloreactive T Cells With
Apoptosis of Bystander Postthymic T Cells Prevents Immune
Reconstitution in Mice With Graft-Versus-Host Disease
Sylvie Brochu,
Benjamin Rioux-Massé,
Jean Roy,
Denis-Claude Roy, and
Claude Perreault
From the Guy-Bernier Research Center, Maisonneuve-Rosemont Hospital,
Montreal, Quebec, Canada.
After hematopoietic stem cell transplantation, the persistence and
expansion of grafted mature postthymic T cells allow both transfer of
donor immunologic memory and generation of a diverse T repertoire. This
thymic-independent process, which is particularly important in humans,
because most transplant recipients present severe thymus atrophy, is
impaired by graft-versus-host disease (GVHD). The goal of this study
was to decipher how GVHD influences the fate of grafted postthymic T
cells. Two major findings emerged. First, we found that, after a brisk
proliferation phase, alloreactive antihost T cells underwent a massive
activation-induced cell death (AICD). For both CD4+ and
CD8+ T cells, the Fas pathway was found to play a major
role in this AICD: alloreactive T cells upregulated Fas and FasL, and
AICD of antihost T cells was much decreased in the case of lpr
(Fas-deficient) donors. Second, whereas non-host-reactive donor T
cells neither upregulated Fas nor suffered apoptosis when transplanted
alone, they showed increased membrane Fas expression and apoptosis when coinjected with host-reactive T cells. We conclude that GVHD-associated AICD of antihost T cells coupled with bystander lysis of grafted non-host-reactive T cells abrogate immune reconstitution by
donor-derived postthymic T lymphocytes. Furthermore, we speculate that
massive lymphoid apoptosis observed in the acute phase of GVHD might be responsible for the occurrence of autoimmunity in the chronic phase of GVHD.
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