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CD4+ T-cell induction of Fas-mediated apoptosis in Burkitt's lymphoma B
cells
EJ Schattner, J Mascarenhas, J Bishop, DH Yoo, A Chadburn, MK Crow and SM Friedman
Department of Medicine, New York Hospital-Cornell Medical Center 10021,
USA.
Cytotoxic function of CD4+ Th1 cells is mediated by Fas (CD95, APO-1) and
its ligand (Fas ligand). Recent studies using nontransformed B cells and
the Ramos Burkitt's lymphoma (BL) B-cell line cells show that CD40 ligation
at the B-cell surface by activated, CD40 ligand (CD40L)- bearing, CD4+ T
cells upregulates Fas expression on B cells and primes B cells for
Fas-mediated death signals. In this work, we examine whether this CD4+
T-cell-dependent molecular pathway for Fas upregulation and B-cell
apoptosis reflects a peculiarity of the Ramos B- cell line or is applicable
to other Burkitt's tumors as well. In 5 of the 6 Epstein-Barr
virus-negative BL cell lines examined, the cells constitutively express
undetectable or low levels of Fas and are resistant to Fas-mediated signals
induced by monoclonal anti-Fas antibody. All 6 of the BL cell line B cells
upregulate Fas in response to CD40 ligation, and in 4 of the cases they
become sensitive to Fas- mediated death signals. In one BL cell line, the
cells are constitutively sensitive to Fas-mediated cytolysis and are
unaffected by CD40 signals. Next, we applied these immunologic
manipulations to cells from a refractory clinical sample and observed that
the tumor cells could be induced to express Fas and undergo apoptosis in
our system. These results establish CD4+ T cells and the Fas-Fas ligand
system as important immune regulators of Burkitt's lymphoma B cells and
indicate that the susceptibility of tumor cells to Fas-mediated death
signals can be modulated by specific activation events at the cell surface.
Volume 88,
Issue 4,
pp. 1375-1382,
08/15/1996
Copyright © 1996 by The American Society of Hematology
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