Abstract:
: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.
journal_name
Bloodjournal_title
Bloodauthors
Mohty M,Jourdan E,Mami NB,Vey N,Damaj G,Blaise D,Isnardon D,Olive D,Gaugler Bdoi
10.1182/blood-2003-09-3220subject
Has Abstractpub_date
2004-06-15 00:00:00pages
4666-8issue
12eissn
0006-4971issn
1528-0020pii
2003-09-3220journal_volume
103pub_type
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