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,¶,
,§
*
Cancer Center and Departments of
Microbiology and Immunology,
Pediatrics, and
§
Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642; and
¶
Eastman Dental Center, Rochester, NY 14620
Normal and malignant CD5+ B lymphocytes can develop
macrophage-like characteristics. One stimulus of this phenotypic shift
is culture of normal mouse splenic B lymphocytes with splenic
fibroblasts or their conditioned media. These biphenotypic B/macrophage
(B/M
) cells simultaneously display macrophage characteristics, such
as phagocytosis and F4/80 expression, while retaining B cell features,
including expression of surface Ig, CD5, B220, and rearranged Ig genes.
The present study investigated the fibroblast-secreted factor that
promotes this phenotypic change from B cell to B/M cell. RT-PCR
analysis demonstrated that mRNA for M-CSF is produced by splenic
fibroblasts. Recombinant M-CSF (CSF-1) could replace
fibroblast-conditioned medium to elicit the development and survival of
B/M cells from splenic B lymphocytes. In addition, neutralization of
fibroblast-secreted M-CSF with specific mAbs abrogated the ability of
conditioned supernatants to promote outgrowth of B/M cells. The
transition from B lymphocyte to B/M cell was marked by the kinetic
appearance of mRNA for the M-CSF receptor, c-fms, at day
3 following culture initiation. These results demonstrate that M-CSF is
important in the development and physiology of mouse B/M cells and
potentially in the growth of human biphenotypic hematological
malignancies. Interestingly, the presence of IFN-
in splenic B
lymphocyte cultures abrogated the effect of fibroblast-conditioned
medium or M-CSF on outgrowth of B/M cells. Furthermore, these
findings suggest that a Th1 microenvironment favored by typical
macrophages is detrimental to the outgrowth of B/M
cells.
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