Nonspecific Immunotherapy Interferon

IFN-a has been a standard therapy for CP CML for nearly two decades. The introduction of imatinib has replaced its role as first line agent, but IFN-a could play a key role in modulating a nonspecific immune-mediated effect toward MRD persisting during imatinib therapy. Several immunologic effects of IFN-a have been documented, including increased expression of adhesion molecules, and enhanced antigen presentation and generation of highly active monocyte-derived DCs (45). Nevertheless, it is still unclear as to which effect is precisely responsible for its antileukemic activity. Recently, the presence of PR3-specific CTLs has been documented in IFN-a-treated patients, but not in imatinib-treated patients. This suggests that IFN-a may enhance the induction of "natural" anti-PR3 CTLs, thus modulating a direct immune-mediated antitumor effect against CML cells (27). Indirect evidence of an underlying immune control of leukemic cells mediated by IFN-a is the fact that some patients maintain CCyR without recurrence of disease for many years after discontinuation of the drug despite persistence of molecular MRD (46). Furthermore, it has recently been observed that 4/7 patients previously exposed to IFN-a maintained CMR for 8 to 13 months after discontinuation of imatinib (47). All these premises provide a novel rationale for employing low doses of IFN-a as promoter of an innate antileukemic immune response both in patients with MRD persisting during imatinib treatment as well as in those patients who have to or wish to stop imatinib after achieving low levels of residual disease.

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