Impaired expression of cell surface receptors for B cell growth factor by
chronic lymphocytic leukemia B cells
RT Perri
Normal human B cell proliferation is controlled by various immunoregulatory
signals including the T cell-derived lymphokine B cell growth factor
(BCGF). The role of BCGF in the regulation of malignant B cell
proliferation is unclear. Therefore, we studied the proliferative response
of purified chronic lymphocytic leukemia (CLL) B cells to BCGF. For all CLL
patients studied, CLL B cells showed a decreased proliferative response as
compared with control B cells for BCGF- induced B cell proliferation
(patient 291 +/- 59 cpm v control 3,942 +/- 622, mean +/- SEM). This
impaired proliferative response appeared to be intrinsic to CLL B cells
since it was not corrected by incubation with increasing concentrations of
BCGF. Attainment of normal B cell responsiveness to BCGF requires the
processing of an initial activation signal which results in the expression
of cell surface receptors for BCGF. Increasing concentrations of the B cell
activation signal (the F(ab')2 fragment of goat anti-human mu chain) did
not improve CLL B cell responsiveness to BCGF. Three-day activated CLL B
cells compared with activated control B cells demonstrated a marked
impairment in their ability to absorb out the BCGF activity present in the
BCGF preparation (BCGF activity absorbed out, patient 12.8% v control 53%).
Pretreatment of CLL B cells with neuraminidase failed to improve either the
proliferative response to BCGF or the expression of cell surface receptors
for BCGF by the CLL B cells. This study suggests that the impaired
responsiveness to BCGF by CLL B cells is the result of impaired expression
of cell surface receptors for BCGF when CLL B cells are exposed to
activation signals.
Volume 67,
Issue 4,
pp. 943-948,
04/01/1986
Copyright © 1986 by The American Society of Hematology
