Involvement of HLA Antigens, Interleukin 2 Receptor and B-Cell Growth Factor in Interferon Action in Hairy Cell Leukemia

Little is known about the mechanism(s) by which alpha-interferon (aIFN), when used as a biotherapeutic agent, suppresses the malignant cells and restores the normal phenotype of cells in patients with hairy cell leukemia (HCL). In previous studies using scanning electron microscopy (SEM) we found that alFN induced unique membrane alterations in target hairy cells in vitro. In addition, aIFN was shown to enhance the expression of HLA class II antigens on HCL cells, to induce the production of new proteins in such cells, and to lower the high levels of soluble IL-2 receptors in the serum of HCL patients. In the light of these results, and the fact that restoration of natural killer cell activity occurs in aIFN-treated patients well after the hematologic profile begins to improve, our studies have focused on the hypothesis that IFNs act directly on the target malignant cells, leading to the elimination of these cells either by inhibiting the proliferation of the malignant cells and/or triggering changes in the differentiation status of the malignant cells that lead to suppression (cytoconversion) of the malignant phenotype. We review the current hypotheses regarding alFN action on leukemic cells, with special reference to its potential antagonism with BCGF