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Normal cellular counterparts of B cell chronic lymphocytic leukemia
AS Freedman, AW Boyd, FR Bieber, J Daley, K Rosen, JC Horowitz, DN Levy and LM Nadler
In an attempt to compare B cell chronic lymphocytic leukemia (B-CLL) with
its normal cellular counterpart, the cell surface phenotype of 100 cases of
B-CLL was determined by using a panel of monoclonal antibodies (MoAbs)
directed against B cell-restricted and -associated antigens. The majority
of B-CLL cells expressed Ia, B4 (CD19), B1 (CD20), B2 (CD21), surface
immunoglobulin (sIg), and T1 (CD5) but lacked C3b (CD35) receptors. In
contrast, the overwhelming majority of small unstimulated B cells expressed
Ia, B4, B1, B2, sIg, and C3b receptors but lacked detectable T1. Small
numbers of weakly sIg+ cells could be identified in peripheral blood and
tonsil that coexpressed the B1 and T1 antigens. Approximately 16% of fetal
splenocytes coexpressed B1, T1, weak sIg, B2, and Ia but lacked C3b
receptors and therefore closely resembled most B-CLL cells. With the
phenotypic differences between the majority of small unstimulated B cells
and B-CLL cells, we examined normal in vitro activated B cells and B-CLL
cells for the expression of B cell-restricted and -associated activation
antigens. Of 20 cases examined, virtually all expressed B5, and
approximately 50% of the cases expressed interleukin-2 receptors (IL-2R)
and Blast-1. Normal B cells were activated with either anti-Ig or
12-0-tetradecanoylphorbol- beta-acetate (TPA) and then were examined for
coexpression of B1, T1, and the B cell activation antigens B5 and IL-2R.
Only cells activated with TPA coexpressed B1 and T1 as well as B5 and
IL-2R. B cells activated with either anti-Ig or TPA proliferated in the
presence of IL- 2, whereas B-CLL cells did not, although they all expressed
the identical 60-kilodalton proteins by immunoprecipitation. These studies
are consistent with the notion that B-CLL resembles several minor
subpopulations of normal B cells including a population of B cells that are
activated in vitro directly through the protein kinase C pathway.
Volume 70,
Issue 2,
pp. 418-427,
08/01/1987
Copyright © 1987 by The American Society of Hematology
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