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 Blood, 16 April 2009, Vol. 113, No. 16, pp. 3813-3820.
Prepublished online as a Blood First Edition Paper on January 26, 2009; DOI 10.1182/blood-2008-07-167189.

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MYELOID NEOPLASIA

ICSBP-mediated immune protection against BCR-ABL–induced leukemia requires the CCL6 and CCL9 chemokines

Valentina Nardi1, Olaia Naveiras1,*, Mohammad Azam1,*, and George Q. Daley1

1 Division of Hematology/Oncology, Children's Hospital Boston and Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, MA

Interferon (IFN) is effective at inducing complete remissions in patients with chronic myelogenous leukemia (CML), and evidence supports an immune mechanism. Here we show that the type I IFNs (alpha and beta) regulate expression of the IFN consensus sequence-binding protein (ICSBP) in BCR-ABL–transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of BCR-ABL–induced leukemia. We identify the chemokines CCL6 and CCL9 as genes prominently induced by the type I IFNs and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression. Insights into the role of these chemokines in the antileukemic response of IFNs suggest new strategies for immunotherapy of CML.


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