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Blood, 15 August 2002, Vol. 100, No. 4, pp. 1449-1453
NEOPLASIA
Blockade of Fas-dependent apoptosis by soluble Fas in LGL
leukemia
Jin Hong Liu,
Sheng Wei,
Thierry Lamy,
Yongxiang Li,
P.K. Epling-Burnette,
Julie Y. Djeu, and
Thomas P. Loughran Jr
From the Hematologic Malignancies and Immunology
Programs, H. Lee Moffitt Cancer Center and Research Institute and the
Veterans Administration Hospital; Departments of Internal Medicine and
Microbiology/Immunology, University of South Florida, College of
Medicine, Tampa, FL
Altered expression of the Fas-Fas ligand apoptotic pathway leads to
lymphoproliferative and autoimmune diseases. In
lpr/lpr mice and children with autoimmune
lymphoproliferative syndrome, defective apoptosis is due to Fas
mutations. Large granular lymphocyte (LGL) leukemia is a clonal
lymphoproliferative disorder associated with rheumatoid arthritis.
Leukemic LGLs are resistant to Fas-dependent apoptosis despite
expressing high levels of Fas. Such resistance can be overcome by
activating leukemic LGLs in vitro, suggesting inhibition of Fas
signaling in leukemic cells. We report that sera from patients with LGL
leukemia contain high levels of soluble Fas. Ten of these 33 patients
with LGL leukemia also had rheumatoid arthritis. Cloning and sequencing
revealed expression of multiple Fas messenger RNA variants in leukemic
LGL. These Fas variants, including 3 newly described here, encode
soluble Fas molecules. Supernatants from cells transfected with these
Fas variants blocked Fas-dependent apoptosis of leukemic LGLs. These
results suggest that blockade of Fas-signaling by soluble Fas may be a
mechanism leading to apoptosis resistance in leukemic LGLs.
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