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 Blood, 7 May 2009, Vol. 113, No. 19, pp. 4681-4689.
Prepublished online as a Blood First Edition Paper on February 27, 2009; DOI 10.1182/blood-2008-05-156471.

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MYELOID NEOPLASIA

Defective homing and impaired induction of cytotoxic T cells by BCR/ABL-expressing dendritic cells

Sabine Mumprecht1, Christina Claus1, Christian Schürch1, Viktor Pavelic1, Matthias S. Matter1, and Adrian F. Ochsenbein1,2

1 Tumor Immunology, Department of Clinical Research, University of Berne, Berne; and 2 Institute for Medical Oncology, Inselspital, Berne, Switzerland

Chronic myelogenous leukemia (CML) is a malignant myeloproliferative disease arising from a hematopoietic stem cell expressing the BCR/ABL fusion protein. Leukemic and dendritic cells (DCs) develop from the same transformed hematopoietic progenitors. How BCR/ABL interferes with the immunoregulatory function of DCs in vivo is unknown. We analyzed the function of BCR/ABL-expressing DCs in a retroviral-induced murine CML model using the glycoprotein of lymphocytic choriomeningitis virus as a model leukemia antigen. BCR/ABL-expressing DCs were found in bone marrow, thymus, spleen, lymph nodes, and blood of CML mice. They were characterized by a low maturation status and induced only limited expansion of naive and memory cytotoxic T lymphocytes (CTLs). In addition, immunization with in vitro–generated BCR/ABL-expressing DCs induced lower frequencies of specific CTLs than immunization with control DCs. BCR/ABL-expressing DCs preferentially homed to the thymus, whereas only few BCR/ABL-expressing DCs reached the spleen. Our results indicate that BCR/ABL-expressing DCs do not efficiently induce CML-specific T-cell responses resulting from low DC maturation and impaired homing to secondary lymphoid organs. In addition, BCR/ABL-expressing DCs in the thymus may contribute to CML-specific tolerance induction of specific CTLs.


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