Background. Since high CD23 expression and release have been reported in B-chronic lymphocytic leukemia (B-CLL), we investigated whether α-interferon or corticosteroids were able to modulate the expression and/or the release of this factor. Methods. CD23 expression was determined with FITC-labelled anti-CD23 monoclonal antibody, and sCD23 release with a sandwich enzyme immunoassay. Twenty-one patients affected by B-CLL (stage A or B) were studied before and after three different treatment regimens (α-interferon, corticosteroids, α-interferon + corticosteroids). Results. CD23 was highly expressed in the B-cells of all patients, and expression was not modified by any of the therapies. sCD23 release from leukemic cells was significantly greater (p <0.00001) in untreated subjects than controls, and in vitro treatment with phorbol myristate acetate (PMA) led to a 10-fold increase (p <0.0001) in sCD23 secretion. On the contrary, PMA did not increase sCD23 release in normal B cells. Treatment with corticosteroids (either alone or associated with α-interferon) reduced sCD23 secretion from leukemic cells, whereas α-interferon alone was not able to modify sCD23 release. Conclusions. Our data support the hypothesis that CD23 plays a role in the maintenance and progression of B-CLL and that the pharmacological modulation of this receptor/lymphokine could be useful in the therapy of B-CLL.
|Number of pages||8|
|Publication status||Published - 1994|
- chronic lymphocytic leukemia
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