The beneficial effects of αIFN in CGL are probably not mediated by NK cells

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Abstract
Natural killer (NK) cells in CGL were measured phenotypically (by Leu7 and CD16 Mab staining) and functionally (by a standard chromium-release cytotoxicity assay) in eight patients before and during .alpha.-IFN therapy. Before .alpha.IFN therapy, phenotypic NK cells were normal in relative and absolute numbers but were consistently defective functionally; this defect was partially corrected by in vitro exposure to .alpha.IFN. During .alpha.IFN therapy, there was no change in NK function in five patients and enhanced (two patients) or reduced (one patient) activity was observed in the other three. Cold-target inhibition experiments showed no evidence of NK binding to normal or CGL myeloid progenitors. It is concluded that .alpha.IFN-enhanced NK function, a known anti-tumour mechanism in animal models, is probably not the basis of the responsiveness of CGL to .alpha.IFN therapy.