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Blood, 1 September 2002, Vol. 100, No. 5, pp. 1795-1801
NEOPLASIA
Protection of CLL B cells by a follicular dendritic cell line is
dependent on induction of Mcl-1
Irene M. Pedersen,
Shinichi Kitada,
Lorenzo M. Leoni,
Juan M. Zapata,
James G. Karras,
Nobuhiro Tsukada,
Thomas J. Kipps,
Yong Sung Choi,
Frank Bennett, and
John C. Reed
From The Burnham Institute, and University of
California San Diego, Dept Medicine, La Jolla, CA; Laboratory
of Cellular Immunology, Ochsner Foundation, New Orleans, LA; and Isis
Pharmaceuticals, Carlsbad, CA.
Chronic lymphocytic leukemia (CLL) B cells have defects in
apoptosis pathways and therefore accumulate in vivo. However, when removed from the patient and cultured in vitro, these malignant cells
rapidly undergo apoptosis. Recent studies suggest that leukemia cell
survival is influenced by interactions with nonleukemia cells in the
microenvironment of lymph nodes, marrow, and other tissues. To model
such cell-cell interactions in vitro, we cultured freshly isolated CLL
B cells with a follicular dendritic cell line, HK. CLL B cells
cocultured with HK cells were protected from apoptosis, either
spontaneous or induced by treatment with anticancer drugs. Protection
against spontaneous apoptosis could also be induced by coculturing the
CLL B cells with normal dendritic cells (DCs) or with a CD40-ligand
(CD154)-expressing fibroblast cell line. Examination of the expression
of several apoptosis-regulatory proteins revealed that coculture with
HK cells or DCs induced up-regulation of the antiapoptotic Bcl-2 family
protein Mcl-1 in CLL B cells, whereas CD40 ligation increased
expression of Bcl-XL. Cell-cell contact was required for
HK-induced protection, and introducing neutralizing antibodies against
various adhesion molecules showed that CD44 was involved in HK-mediated
survival, whereas CD40, intercellular adhesion molecule-1
(ICAM-1) and vascular cell adhesion molecule-1
(VCAM-1) were not. Anti-CD44 antibodies also blocked Mcl-1
induction by HK cells. Mcl-1 antisense oligonucleotides reduced
leukemia cell expression of Mcl-1, and significantly suppressed HK-induced protection against apoptosis, whereas control
oligonucleotides had no effect. Thus, HK cells protect CLL B cells
against apoptosis, at least in part through a CD44-dependent mechanism
involving up-regulation of Mcl-1, and this mechanism is distinct from
that achieved by CD40 ligation. Consequently, the particular
antiapoptotic proteins important for CLL survival may vary depending on
the microenvironment.
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