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Departments of
*
Microbiology and Immunology,
Medicine, and
Anatomy, Division of Immunobiology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA 23298
The observation that follicular dendritic cells (FDC) reduce
apoptosis in B cells prompted the hypothesis that FDC might enhance
tumor cell survival by protecting malignant B cells from apoptotic
death. To test this notion, apoptosis was induced in B cell lymphomas
by anti-Fas or various antineoplastic agents in the presence and
absence of FDC. Apoptosis was detected and quantified by TUNEL
analysis. Induction of apoptosis with anti-Fas, etoposide,
cyclophosphamide, and busulfan was markedly antagonized by FDC at FDC
to B cell ratios of
1:16. For example, treatment with 10 ng/ml
anti-Fas caused 6090% of A20 cells to undergo apoptosis in
6 h, whereas addition of FDC reduced apoptosis to background
levels (315%). Similarly, treatment with busulfan induced apoptosis
in 5580% of A20 cells, whereas addition of FDC reduced B cell death
to
15%; moreover, depletion of FDC abrogated the protective actions.
In contrast, the apoptosis-inducing effect of Adriamycin was not
reversed by FDC. The ability to block apoptosis induced by anti-Fas
or busulfan was not limited to A20 but was observed in four other
malignant pre-B cell or B cell lines. The mechanism by which FDC spare
malignant B cells from apoptosis did not involve alterations in levels
of Bcl-2, Bcl-XL, or Bax. Collectively, these data raise
the possibility that FDC may enhance tumor cell survival by protecting
malignant B cells against apoptosis induced by anti-Fas and some
but not all chemotherapeutic agents.
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