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Blood, Vol. 94 No. 9 (November 1), 1999:
pp. 3135-3140
Membrane-Bound Fas (Apo-1/CD95) Ligand on Leukemic Cells: A
Mechanism of Tumor Immune Escape in Leukemia Patients
Agnès Buzyn,
Frederic Petit,
Marina Ostankovitch,
Suzanne Figueiredo,
Bruno Varet,
Jean-Gérard Guillet,
Jean-Claude Ameisen, and
Jérôme Estaquier
From the INSERM Unité 445, ICGM, Hôpital Cochin; INSERM E
99-22, Faculté de Médecine Bichat; and Service
d'Hématologie Adultes, Hôpital Necker-Enfants Malades,
Paris, France.
There is evidence from bone marrow transplantation that T cells may
be involved in the immunologic control of leukemia. But many patients
relapse despite a potent graft-versus-leukemia effect mediated by
allogeneic T cells. The expression of the FasL protein has been
suggested as a mechanism of tumor immune escape. We, therefore,
evaluated the capacity of leukemic cells from patients with acute or
chronic myelogenous leukemia to escape the allogeneic or autologous
immune response by bearing the FasL molecule. Although almost all
leukemic cells express the 37-kD form of FasL, only 54% of acute
myeloblastic leukemia and 27% of chronic myeloid leukemia (CML) cells
bore a FasL with killing properties, as assessed by the ability of
leukemic cells to cause the apoptosis of a Fas-sensitive target cell
line or autologous activated T cells in 3 tested leukemic cases.
Experiments with a recombinant Fas-Fc molecule confirmed the role of
Fas/FasL in leukemic-mediated cell death. Only CML leukemic cells from
certain individuals contained the 26-kD truncated form of FasL. Thus,
myeloid leukemic cells from some, but not all patients can set up a
mechanism of immune escape involving the Fas/FasL pathway. This
leukemic escape may have implications for patients eligible for
adoptive cellular immunotherapy.
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