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Blood, 15 June 2004, Vol. 103, No. 12, pp. 4666-4668.
Prepublished online as a Blood First Edition Paper on January 8, 2004; DOI 10.1182/blood-2003-09-3220.
Submitted September 22, 2003
Accepted December 24, 2003
Imatinib and plasmacytoid dendritic cell function in chronic myeloid leukemia patients
Mohamad Mohty, Eric Jourdan, Naira Ben Mami, Norbert Vey, Ghandi Damaj, Didier Blaise, Daniel Isnardon, Daniel Olive, and Beatrice Gaugler*
Institut Paoli-Calmettes, Marseille, France
Service de Medecine Interne B, CHU de Nimes, Nimes, France
* Corresponding author; email: mdmohty{at}aol.com.
Plasmacytoid dendritic cells (PDCs) are crucial effectors in innate immunity. In this study, we show that imatinib, a potent inhibitor of BCR/ABL tyrosine kinase activity, in the presence of Flt3-Ligand, could induce CD34+ progenitors from chronic myeloid leukemia (CML) to give rise in vitro to typical BDCA-2+ type I interferon-producing PDCs. The impact of imatinib on PDC generation was related to upregulation of Flt3 on leukemic CD34+ progenitors. Moreover, CML patients who were in complete cytogenetic or molecular response after imatinib treatment restored their blood PDCs both quantitatively and functionally comparable to healthy donors, in contrast to patients not responding to imatinib, further confirming that disease response to imatinib is accompanied by restoration of PDC function in vivo. These findings provide evidence that response to imatinib is capable to restore some DC-related immune functions in CML that might be beneficial for long term disease control.
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