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S Fournier, M Rubio, G Delespesse and M Sarfati
Allergy Research Laboratory, Notre-Dame Hospital Research Center,
University of Montreal, Canada.
CD23 gene is overexpressed and abnormally regulated in the most frequent
adult leukemic disorder, B chronic lymphocytic leukemia (B- CLL). Switch on
and off in the upregulation of surface CD23 expression consistently occurs
in the early stage of normal B-cell activation, suggesting a key role for
CD23 in this process. We show here that, after ligation of mlg in the
presence of interleukin-4, the increase of CD23 protein precedes B-cell DNA
synthesis and mainly results from the strong induction of CD23 type-B
isoform. Exposure of normal B cells to conventional or
phosphorothioate-derivatized CD23 antisense oligonucleotides (predominantly
type B) significantly augments B-cell proliferation induced by antigen
receptor stimulation or direct contact with activated T cells.
Unexpectedly, CD23 antisense, but not sense, oligonucleotides specifically
enhance rather than suppress CD23 expression on B cells. Finally, a
selective increase in CD23 type-B expression provokes the entry of resting
(Go) CLL B cells into G1 and S phase of the cell cycle in the absence of
any other stimulus, whereas it synergizes with tumor necrosis factor-alpha
to increase the number of activated B cells. These results provide
compelling evidence that CD23 represents an important molecule directly
involved in the process of normal or leukemic B-cell activation and growth.
This article has been cited by other articles:
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| Copyright © 1994 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
