In chronic myeloid leukemia (CML), BCR-ABL-mediated oncogenic signaling can be 
successfully targeted with the BCRABL- inhibitors imatinib, nilotinib, and 
dasatinib leading to complete cytogenetic (Philadelphia chromosome not 
detectable upon cytogenetic testing of bone marrow) and even complete molecular 
(BCR-ABL not detectable by PCR in peripheral blood) responses. However, CML 
apparently can not be cured by BCR-ABL inhibitors alone, likely due to 
treatment-resistance of CML stem/progenitor cells, which provokes a relapse of 
disease after cessation of therapy. Evidence from patients treated with 
allogenic stem cell transplantation or IFN-α points to an important role of 
anti-tumor immunity for durable control of CML disease. Data from multiple in 
vitro and ex vivo studies indicate that BCR-ABL inhibitors may also influence 
anti-tumor immunity. Varying effects on different immune effector cell subsets 
and of the different compounds have been reported, the latter being due to their 
particular and diverse potency and spectrum of target kinases. As multiple 
approaches presently aim to combine BCR-ABL inhibition with immunotherapeutic 
strategies to improve disease control in CML, immunomodulatory effects of the 
available BCR-ABL inhibitors may be of direct clinical relevance. Here we review 
the available data regarding the effects of imatinib, nilotinib, and dasatinib 
on dendritic cells, T cells and natural killer cells as important cellular 
components of anti-tumor immunity.