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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.
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NEOPLASIA Brief report
Imatinib and plasmacytoid dendritic cell function in patients with chronic myeloid leukemia
Mohamad Mohty,
Eric Jourdan,
Naira Ben Mami,
Norbert Vey,
Ghandi Damaj,
Didier Blaise,
Daniel Isnardon,
Daniel Olive, and
Béatrice Gaugler
From the Laboratoire d'Immunologie des Tumeurs, Institut Paoli-Calmettes, Marseille, France; Unité de Transplantation et de Thérapie Cellulaire (UTTC), Institut Paoli-Calmettes, Marseille, France; Service de Médecine Interne B, Centre Hospitalier et Universitaire (CHU) de Nimes, Nimes, France; Département d'Hématologie, Institut Paoli-Calmettes, Marseille, France; and Institut National de la Santé et de la Recherche Médicale (INSERM) U119, Marseille, France.
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 effect of imatinib on PDC generation was related to up-regulation of Flt3 on leukemic CD34+ progenitors. Moreover, patients with chronic myeloid leukemia (CML) 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. (Blood. 2004;103:4666-4668)

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